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<rss version="2.0"><channel><title>Neue Studien: Europe PMC</title><link>https://www.psoriasis-news.de/articles.html/1_articles/page/3/?d=1</link><description>Neue Studien: Europe PMC</description><language>de</language><item><title>Efficacy and Safety of Tildrakizumab for Treatment of Moderate-to-Severe Scalp Psoriasis in Patients with Obesity Over 52 Weeks.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/efficacy-and-safety-of-tildrakizumab-for-treatment-of-moderate-to-severe-scalp-psoriasis-in-patients-with-obesity-over-52-weeks-r610/</link><description><![CDATA[<h4>Introduction</h4>Obesity contributes to inflammation and may decrease psoriasis treatment efficacy. We investigated whether obesity affects the efficacy and safety of tildrakizumab, an anti-interleukin-23 p19 antibody approved for the treatment of adults with moderate-to-severe plaque psoriasis, for scalp psoriasis treatment.<h4>Methods</h4>This was a subgroup analysis of a randomized, double-blind, placebo-controlled, Phase 3b trial in patients with moderate-to-severe plaque psoriasis affecting the scalp. Patients receiving tildrakizumab 100 mg or placebo were analyzed by baseline obesity status (body mass index ≥ 30 versus &lt; 30 kg/m<sup>2</sup>). Efficacy outcomes included an Investigator Global Assessment (IGA) modified 2011 (scalp) (IGA mod 2011 [scalp]) score of "clear"/"almost clear" (0/1) with a ≥ 2-point reduction (IGA mod 2011 [scalp] response), ≥ 90% improvement in Psoriasis Scalp Severity Index (PSSI) score (PSSI 90 response), ≥ 4-point reduction in Scalp Itch-Numeric Rating Scale (Scalp Itch-NRS response; among patients scoring ≥ 4 at baseline), and percent change from baseline (%CFB) in affected scalp surface area (SSA). Safety was assessed from adverse events. The analysis was not prospectively powered to detect differences between subgroups.<h4>Results</h4>In the intention-to-treat population, 56/117 (47.9%) patients randomized to tildrakizumab and 57/114 (50.0%) to placebo had obesity (modified intention-to-treat population: tildrakizumab, 43/89 [48.3%]; placebo, 40/82 [48.8%]). At Week 16, significantly more patients treated with tildrakizumab versus those receiving placebo achieved IGA mod 2011 (scalp) (obesity, 21/43 [48.8%] versus 4/40 [10.0%], p = 0.0002; no obesity, 23/46 [50.0%] versus 2/42 [4.8%], p &lt; 0.0001) and PSSI 90 responses (obesity, 27/43 [62.8%] versus 4/40 [10.0%], p &lt; 0.0001; no obesity, 27/46 [58.7%] versus 0/42 [0.0%], p &lt; 0.0001). Treatment effect was also maintained for Scalp Itch-NRS response (p &lt; 0.0001) and mean %CFB in affected SSA (no statistical testing), regardless of obesity status. Results in patients treated with tildrakizumab were similar through Week 52. No new safety signals were identified.<h4>Conclusions</h4>No statistically significant differences in efficacy or safety were observed between patients with and without obesity.<h4>Clinicaltrials</h4><h4>Gov identifier</h4>NCT03897088.<p><a href="http://europepmc.org/article/MED/42105056?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">610</guid><pubDate>Thu, 14 May 2026 18:05:26 +0000</pubDate></item><item><title>The role of biosimilars in enhancing global access to psoriasis treatment.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/the-role-of-biosimilars-in-enhancing-global-access-to-psoriasis-treatment-r608/</link><description><![CDATA[The introduction of biosimilars for moderate-to-severe psoriasis treatment has demonstrated comparable efficacy and safety to originator biologics, with the potential to improve cost-effectiveness. We explored the potential for biosimilars to improve access to biologics for psoriasis, especially in low-and-middle-income countries where costs often limit access to originators. The analysis was based on a systematic review conducted as part of the submission process to include adalimumab and ustekinumab in the World Health Organization Essential Medicines List for psoriasis. Among 17 studies included in the systematic review, we focused on those that provided data evaluating the cost and/or cost-effectiveness of biosimilars versus originators in the treatment of psoriasis. Two studies met the inclusion criteria. The first was a cohort-based Markov model which showed that biosimilar adalimumab was cost-effective compared with originator adalimumab for moderate-to-severe psoriasis. The second, using a cost-per-responder model, found that adalimumab biosimilar had the lowest cost-per psoriasis area and severity index (PASI) complete clearance (PASI100) responder among the anti-tumor necrosis factor therapies. Biosimilars have a key role in reducing costs and expanding treatment availability for psoriasis patients. Further health economic studies, focusing on psoriasis, are required to demonstrate how biosimilars can improve access to biologics in this condition.<p><a href="http://europepmc.org/article/MED/42002071?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">608</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Identification and clinical implications of immune-related hub genes in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/identification-and-clinical-implications-of-immune-related-hub-genes-in-psoriasis-r607/</link><description><![CDATA[<h4>Background</h4>Psoriasis, a chronic inflammatory skin disease affecting 2-3% of the global population, is driven by dysregulated immune responses. Despite advancements in biologic therapies, treatment challenges persist due to high recurrence rates. This study aimed to identify immune-related hub genes and elucidate their clinical implications in psoriasis pathogenesis and therapy.<h4>Methods</h4>Multiple microarray datasets from psoriasis patients (GSE30999, GSE106992, GSE14905, GSE78097, and GSE117468) were obtained to identify immune-key genes by differential gene analysis and Weighted Gene Co-expression Network Analysis (WGCNA). Subsequently, immune-related hub genes were identified using the Least Absolute Shrinkage and Selection Operator (LASSO) algorithm and Protein-Protein Interaction (PPI) networks, with further validation through Gene Set Enrichment Analysis (GSEA) and Receiver Operating Characteristic (ROC) curves to assess exploratory within-sample discrimination. Pearson correlation analysis evaluated the relationship between hub genes, skin lesion severity, and treatment outcomes. The study also conducted immune infiltration by using the Cell-type Identification by Estimating Relative Subsets Of RNA Transcripts (CIBERSORT) algorithm and identified potential therapeutic targets by the Drug-Gene Interaction Database (DGIdb).<h4>Results</h4>Thirty-one immune-related key genes were identified, and six hub genes (CLEC7A, CXCL1, IRF1, S100A12, S100A8, S100A9) were validated as central players in immune signaling pathways. These genes exhibited within-sample discrimination (AUC &gt; 0.9) and correlated with disease severity and biological therapy efficacy. Immune infiltration analysis revealed increased activated memory CD4+ T cells and M1 macrophages in lesional skin, which was strongly associated with hub gene expression. Additionally, drug-gene interaction analysis identified potential therapeutic agents targeting these genes.<h4>Conclusion</h4>This study identified six immune-related hub genes that were closely linked to the severity of psoriasis, the effectiveness of biological treatments, and infiltrated activated memory CD4+ T cells and M1 macrophages. Our findings elucidate a novel immune-related hub gene network in psoriasis and provide potential targets for the development and application of biologics.<p><a href="http://europepmc.org/article/MED/42008507?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">607</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Update on the Etiology and Pathogenesis of Erythrodermic Psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/update-on-the-etiology-and-pathogenesis-of-erythrodermic-psoriasis-r606/</link><description><![CDATA[Erythrodermic psoriasis(EP) is a rare, life-threatening variant affecting 75%-90% of the body surface area. Characterized by widespread erythema and potential systemic symptoms like fever and lymphadenopathy, it severely impairs patient quality of life. The pathogenesis of erythrodermic psoriasis is not fully understood. It is a multifactorial, multistep process suspected to result from an abnormal immune response induced by both genetic and environmental factors. Key contributors to erythrodermic psoriasis onset include specific gene polymorphisms, altered expression of adhesion molecules, dysregulated cytokine activity, and abnormal activation of T cell subsets. Additionally, imbalances in the skin microbiota and external factors, such as infections and medications, play important roles in disease onset and progression. Distinct from prior reviews that primarily emphasize clinical features and treatment, this review integrates recent mechanistic advances across genetic, immune, environmental, and microbiome domains to provide an updated, systems-level framework for understanding erythrodermic psoriasis and to highlight potential therapeutic implications.<p><a href="http://europepmc.org/article/MED/41982475?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">606</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Proliferation-associated protein 2G4 promotes keratinocyte proliferation and survival in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/proliferation-associated-protein-2g4-promotes-keratinocyte-proliferation-and-survival-in-psoriasis-r605/</link><description><![CDATA[<h4>Background</h4>Psoriasis is a non-communicable inflammatory skin disease that affects approximately 2%-3% of the world's population. Given its high impact on quality of life and the fact that a subset of patients exhibits suboptimal or secondary loss of response to current treatments, identifying new therapeutic strategies is crucial. Proliferation-associated protein 2G4 (PA2G4) is a transcription factor that has been exclusively studied in cancer research, where it promotes cell growth and enhances tumourigenesis by inhibiting apoptosis. However, its role in inflammatory skin diseases remains largely unknown.<h4>Objectives</h4>This study focused on the pathophysiological and immunological functions of PA2G4 in psoriasis and evaluated its potential as a therapeutic target.<h4>Methods</h4>Bulk, single-cell, and spatial RNA sequencing combined with immunohistochemistry were used to assess PA2G4 expression in psoriatic skin compared with that in non-lesional controls. Functional studies were performed in primary human keratinocytes and reconstructed human epidermis (RHE) models using the CRISPR/Cas9-mediated knockout (KO) of PA2G4 and pharmacological inhibition of PA2G4 with the small-molecule WS6. The regulatory effects of PA2G4 on cellular processes, such as proliferation, differentiation, and survival, were investigated using RNA-seq, western blot analysis, scratch assays, and annexin V staining.<h4>Results</h4>PA2G4 was highly abundant in psoriasis, and its expression was predominantly restricted to basal proliferating keratinocytes. Its gene expression is positively correlated with psoriasis severity, the degree of acanthosis, neutrophil infiltration, and genes which are upregulated in psoriasis. PA2G4 KO in primary human keratinocytes activated differentiation pathways while suppressing proliferation pathways, resulting in the downregulation of proliferation- and inflammation-related genes (e.g. MKI67, IL20, VEGFA, and HIF1A) and the upregulation of differentiation and cell adhesion markers (e.g. KRT6C, LCE2C, and DSG4). Functionally, the PA2G4 KO reduced keratinocyte proliferation in scratch assays, attenuated interleukin-22-induced acanthosis in RHE models, and promoted keratinocyte death. Pharmacological inhibition of PA2G4 using the small-molecule inhibitor WS6 similarly downregulated genes associated with proliferation and cell survival.<h4>Conclusions</h4>PA2G4 could promote keratinocyte hyperproliferation and survival in psoriasis, thereby critically influencing epidermal homeostasis. Therefore, inhibition of PA2G4 may represent a new treatment option for psoriasis.<p><a href="http://europepmc.org/article/MED/42008715?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">605</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Retrospective Analysis of Inflammatory Parameters and Vitamins' Levels in Psoriasis Patients: A Case-Control Study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/retrospective-analysis-of-inflammatory-parameters-and-vitamins-levels-in-psoriasis-patients-a-case-control-study-r604/</link><description><![CDATA[<h4>Introduction</h4>Psoriasis is a chronic immune-mediated inflammatory disorder affecting both adults and children worldwide, with an average prevalence of approximately 2%. Recent evidence suggests that several hematological inflammatory parameters and vitamin levels may serve as accessible biomarkers for disease activity and severity assessment.<h4>Methods</h4>This single-center retrospective case-control study was conducted at Jordan University Hospital using electronic medical record data from January 2019 to December 2023. The study included 142 patients with psoriasis and 277 age- and sex-matched controls. Psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). Hematological inflammatory indices-including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII)-as well as vitamin D and vitamin B12 levels were evaluated.<h4>Results</h4>The mean age ± standard deviation was 43.76 ± 16.78 years, with no significant differences between psoriasis cases and controls. Females accounted for 54.93% of psoriasis cases compared with 54.41% of controls. The mean PASI score was 9.02 ± 9.00. Approximately 51.79% of psoriasis patients were vitamin D deficient, while 17.82% had vitamin B12 deficiency. No significant differences in psoriasis severity categories were observed across vitamin B12 or vitamin D levels (p = 0.808 and p = 0.184, respectively). The mean NLR, PLR, and SII were 2.21, 124.6, and 588,441.8, respectively. These inflammatory indices did not demonstrate statistically significant differences between psoriasis patients and controls (p &gt; 0.05).<h4>Conclusion</h4>No significant associations were observed between psoriasis severity and inflammatory hematological indices (NLR, PLR, SII) or vitamin deficiencies. These findings suggest limited standalone utility of these biomarkers for routine assessment of psoriasis severity in this retrospective cohort.<p><a href="http://europepmc.org/article/MED/41993888?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">604</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Cell-type-specific causal effects of CEBPD in CD8&#x2009;+&#x2009;S100B&#x2009;+&#x2009;Tcells and ZFP36 in monocytes modulate the protective and risk phenotypes in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/cell-type-specific-causal-effects-of-cebpd-in-cd8%E2%80%89%E2%80%89s100b%E2%80%89%E2%80%89tcells-and-zfp36-in-monocytes-modulate-the-protective-and-risk-phenotypes-in-psoriasis-r603/</link><description><![CDATA[Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by dysregulated keratinocyte proliferation, immune cell infiltration, and systemic comorbidities. Despite the identification of numerous genetic susceptibility loci for psoriasis through genome-wide association studies (GWAS), their functional roles and underlying causal contributions to psoriasis pathogenesis remain largely unclear. Integrating multi-omics data with causal inference approaches, such as Mendelian randomization (MR), represents a promising strategy for addressing this gap and identifying key regulatory genes. We integrated transcriptome data from the Gene Expression Omnibus database (GEO) database (GSE14905 and GSE30999) and performed weighted gene co-expression network analysis and differential expression analysis to identify psoriasis-related genes. Protein-protein interaction networks and four centrality algorithms (Maximal Clique Centrality (MCC), Maximum Neighborhood Component (MNC), Edge Percolated Component (EPC), and Degree centrality) were applied to identify hub genes, and machine learning methods (least absolute shrinkage and selection operator regression, Random Forest, and artificial neural network) were used to screen diagnostic biomarkers. Immune infiltration analysis was performed using CIBERSORT, and the causal association of signature genes with psoriasis was examined using two-sample MR with single-cell expression quantitative trait locus data from the OneK1K cohort and GWAS summary statistics from FinnGen. Module genes that were significantly associated with psoriasis were identified in our study, among which 19 hub genes were screened. Using machine learning approaches, we further refined these findings to seven signature genes. The diagnostic model based on these seven genes achieved an area under the curve of 0.980. Immune infiltration analysis revealed strong associations between CCAAT/enhancer-binding protein delta (CEBPD) and activated CD4 + memory T cells and follicular helper T cells, and between zinc finger protein 36 (ZFP36) and M1 macrophages. MR analysis demonstrated that higher CEBPD expression in CD8 + S100B + T cells was protective (odds ratio [OR] = 0.795, P = 0.015), whereas higher expression of the ZFP36 gene in monocytes was a risk factor (OR = 1.214, P = 0.043) for psoriasis. Our study identified a robust seven-gene signature with high diagnostic accuracy for psoriasis and provided genetic evidence for the cell type-specific causal role of CEBPD and ZFP36. These findings enhance our understanding of psoriasis pathogenesis and suggest potential targets for developing cell-selective immunomodulatory therapies.<p><a href="http://europepmc.org/article/MED/41991682?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">603</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Wogonin attenuates psoriasis through anti-inflammatory effects by inhibiting reactive oxygen species production and the AKT/NF-&#x3BA;B signaling pathway.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/wogonin-attenuates-psoriasis-through-anti-inflammatory-effects-by-inhibiting-reactive-oxygen-species-production-and-the-aktnf-%CE%BAb-signaling-pathway-r602/</link><description><![CDATA[Psoriasis is a common, chronic, inflammatory skin disease that affects many patients and exerts a heavy physical and mental burden. Wogonin (WG), derived from the root extract of Scutellaria Baicalensis, has shown therapeutic effects in a variety of inflammatory diseases. However, its specific effects and mechanisms in psoriasis treatment remain poorly understood. This study aimed to investigate the therapeutic effects and underlying mechanisms of WG in psoriasis. In this study, we first identified potential therapeutic targets of WG for psoriasis by intersecting the corresponding targets of psoriasis and WG, then performed Protein-Protein Interaction (PPI) network analysis and enrichment analyses. Next, we employed Cytoscape to identify potential key targets and performed molecular docking to predict possible targets. M5-induced HaCaT cells and imiquimod (IMQ)-mouse models were used to explore the effects and mechanisms. Bioinformatic analyses indicated that WG may exert anti-inflammatory effects through inhibiting PI3K/AKT pathway activation and oxidative stress. In vitro results showed that WG suppressed the increase of pro-inflammatory cytokine expression levels, reactive oxygen species (ROS) level, phosphorylation of Akt and p65, and several key target mRNA expression levels induced by M5 stimulation. Oral administration of WG remarkably alleviated psoriatic like lesions in IMQ-induced mice, inhibited inflammatory cytokines and Ki-67 expression level in mouse skin lesions. Our results indicate that WG exhibits significant anti-inflammatory effects in psoriasis by suppressing reactive oxygen species (ROS) production and inhibiting the AKT/NF-κB signaling pathway. These results highlight WG's potential as a promising therapeutic agent for psoriasis treatment.<p><a href="http://europepmc.org/article/MED/42000881?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">602</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/role-of-the-stat3-signaling-pathway-in-cell-proliferation-and-inflammation-in-psoriasis-and-approaches-for-targeted-therapies-a-review-r601/</link><description><![CDATA[Psoriasis is a common chronic inflammatory skin disease with a complex pathogenesis that involves the dysregulation of multiple cellular components and interconnected molecular pathways. Signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that integrates signals from multiple cytokines and growth factors to regulate gene expression involved in cell proliferation, survival, and inflammation. Emerging evidence has shown the pivotal role of STAT3 in driving the persistent inflammatory state and aberrant keratinocyte behavior characteristic of psoriasis. This review systematically summarizes the fundamental biological functions of STAT3 (including its phosphorylation, dimerization, and nuclear translocation processes) and its intrinsic mechanism of action in the pathological process of psoriasis. We focus on the critical regulatory role of STAT3 in psoriasis-related inflammatory signaling networks, detailing how it modulates the expression of pro-inflammatory mediators to influence abnormal immune responses and pathological keratinocyte proliferation in lesional skin. Furthermore, the review comprehensively evaluates the latest developments in STAT3-based targeted therapeutic strategies, including small-molecule inhibitors (eg, WB518 and quinone derivatives), biologics, and nucleic acid-based approaches (eg, siRNA and miRNA delivery systems), analyzing their efficacy, safety profiles, and potential clinical applications in current and future treatment regimens. By synthesizing findings from numerous experimental and clinical studies, we aim to address the existing research gap regarding the precise specific regulatory mechanisms of STAT3 and its translational therapeutic implications in psoriasis, providing a foundation for the development of more effective and personalized therapeutic interventions for this condition.<p><a href="http://europepmc.org/article/MED/42015469?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">601</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>The Effectiveness of Probiotics in Psoriasis: An Umbrella Review.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/the-effectiveness-of-probiotics-in-psoriasis-an-umbrella-review-r600/</link><description><![CDATA[<h4>Background</h4>Psoriasis is an immune-mediated inflammatory skin condition that is chronic and causes a great deal of disease burden, especially for those affected in their most productive years. Gut microbiota, immune parameters and, in turn, psoriasis symptom improvement have recently been associated with the use of probiotics in several different studies.<h4>Objectives</h4>This study aims to conduct an umbrella review of systematic reviews and meta-analyses of the effectiveness of probiotic supplementation as a possible adjuvant in the treatment of psoriasis.<h4>Methods</h4>This umbrella review is listed in the PROSPERO database (registration number CRD420251130518) and was referenced according to the PRISMA 2020 guidelines. The data were obtained after a systematic search of the literature in Cochrane, Scopus and PubMed. The quality of the methodology was evaluated using the AMSTAR 2 tool; the overlap was evaluated with the corrected covered area (CCA) method.<h4>Discussions</h4>Five systematic reviews and meta-analyses were included, covering hundreds of adult psoriasis patients. The probiotics studied consisted of both single-strain and multistrain formulations, sometimes combined with prebiotics. Probiotics are associated with significantly reduced Psoriasis Area and Severity Index (PASI) scores, increased PASI 75 response rates, lowered inflammatory biomarkers (CRP, TNFα, IL-6) and improved Dermatology Life Quality Index (DLQI). Greater effectiveness was found with multistrain probiotics, treatment duration of ≥ 12 weeks and studies conducted in Asia. Most studies reported good safety and minimal side effects. However, a high overlap among included reviews was observed (CCA = 38.64%), which should be considered when interpreting the findings and their limitations.<h4>Conclusions</h4>Probiotics, particularly multistrain formulations, show potential as a safe and effective adjuvant therapy for reducing psoriasis severity and improving patient quality of life. Further clinical trials are needed to identify the most effective strains and optimal duration of treatment.<p><a href="http://europepmc.org/article/MED/42005309?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">600</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Nanotechnology advances for psoriasis treatment and future prospects.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/nanotechnology-advances-for-psoriasis-treatment-and-future-prospects-r599/</link><description><![CDATA[Psoriasis is a chronic, immune-mediated disorder with strong genetic susceptibility and environmental triggers, characterized by excessive proliferation of keratinocytes and recruitment of inflammatory cells. Affecting 2-3% of the global population and represents a significant public health challenge. In psoriasis, the skin barrier is altered rather than uniformly enhanced, and its permeability varies with drug types and disease states, which may affect the effective delivery of drugs to affected areas. Nanotechnology demonstrates potential in drug delivery, protecting drug molecules from degradation, enabling targeted therapy, and reducing side effects, thereby improving pharmacokinetics and enhancing the bioavailability of therapeutic agents. This review specifically examines the emergence of multimodal nanotherapeutic approaches, which defined as the strategic integration of two or more distinct therapeutic modalities (e.g., pharmacotherapy paired with phototherapy, gene editing, or RNA interference) within a unified nanocarrier platform to achieve synergistic efficacy. By systematically evaluating these advanced combinatory strategies, this review provides a distinct perspective compared to existing literature, which predominantly focuses on conventional, single-mode drug delivery systems. To this end, it reviews nanotechnology combined with multiple therapies and introduces the current advantages and disadvantages of integrating nanotechnology with conventional anti-psoriatic drugs Finally, it presents the challenges and prospects of using nanotechnology to treat psoriasis and provides reliable solutions for its clinical management. Overall, this review advances psoriasis treatment toward precision and efficiency, revealing the broad prospects of nanomedicine in conquering this intractable disease.<p><a href="http://europepmc.org/article/MED/41984395?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">599</guid><pubDate>Thu, 23 Apr 2026 06:10:08 +0000</pubDate></item><item><title>Majoon Ushba alleviated IL-17A sensitized keratinocyte ferroptosis via JAK-2-STAT-3 signaling axis and reversed imiquimod induced psoriasiform inflammation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/majoon-ushba-alleviated-il-17a-sensitized-keratinocyte-ferroptosis-via-jak-2-stat-3-signaling-axis-and-reversed-imiquimod-induced-psoriasiform-inflammation-r598/</link><description><![CDATA[Psoriasis is a relapsing autoimmune disease exacerbated by aberrant interleukin (IL)-17 A activity. Majoon Ushba, a unani polyherbal formulation implicated in clinical cases of psoriasis lacks immunopharmacological validation. The study aims to investigate the pre-clinical efficacy of Majoon Ushba and its therapeutic role in mitigating IL-17A-induced keratinocytes ferroptosis via ablation of JAK-2/STAT-3 pathway. HaCaT cells were stimulated with IL-17A to assess the activation of the JAK-2-STAT-3 pathway. The STAT-3 inhibitor, S3I-201, was used to confirm the role of the STAT-3 axis in keratinocyte ferroptosis. Majoon Ushba pretreatment was assessed to determine its efficacy in alleviating keratinocyte ferroptosis. An imiquimod (IMQ)-induced psoriasis mouse model was used to evaluate the pre-clinical efficacy of Majoon Ushba. Furthermore, prior high-performance liquid chromatography (HPLC) profiling was leveraged for in-silico docking analysis to identify the binding affinities of key phytoconstituents with IL-17RA and STAT-3. Majoon Ushba alleviated the IL-17A/JAK-2-STAT-3 axis, improved GPX4 expression, and regulated lipid peroxidation. Subsequently, Majoon Ushba also reversed the expression of pathogenic mediators and led to a reduction in serum cytokine levels of IL-17A, IL-23, and IFN-γ. An in-silico docking analysis suggested favorable binding affinities for key phytoconstituents of Majoon Ushba against IL-17RA and STAT-3. Aligned with pre-clinical and in vitro results, the computational findings offer initial evidence that the polyherbal formulation may influence the IL-17A/JAK-2-STAT-3 signaling pathway. In conclusion, our preliminary findings reveal a plausible mechanistic basis for the anti-psoriatic efficacy of Majoon Ushba, warranting larger clinical trials in psoriasis patient cohorts.<p><a href="http://europepmc.org/article/MED/41973793?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">598</guid><pubDate>Tue, 14 Apr 2026 07:47:06 +0000</pubDate></item><item><title>Efficacy and safety of ustekinumab biosimilars for treating moderate-to-severe plaque psoriasis: a systematic review and network meta-analysis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/efficacy-and-safety-of-ustekinumab-biosimilars-for-treating-moderate-to-severe-plaque-psoriasis-a-systematic-review-and-network-meta-analysis-r597/</link><description><![CDATA[To compare the efficacy and safety of different ustekinumab biosimilars for treating moderate-to-severe plaque psoriasis (PP), providing an evidence-based basis for clinical medication. We systematically searched randomized controlled trials on ustekinumab biosimilars for treating moderate-to-severe PP in adults from Embase, PubMed, Cochrane Library, and Web of Science. Stata 18.0 was utilized for data analysis. Nine studies were included, involving 4293 moderate-to-severe PP patients. 1) Ustekinumab biosimilars and the reference listed drug (RLD) ustekinumab-RP had no significant difference in the psoriasis area and severity index (PASI) improvement (P &gt; 0.05), and the biosimilar CT-P43 was most effective in improving PASI at different time points. 2) For the dermatology life quality index, Bmab1200, AVT04 and CT-P43, had statistically significant differences from the RLD (P &lt; 0.05). 3) The biosimilar CT-P43 was most effective in improving the Physician Global Assessment score, with the highest SUCRA value (99.8%). 4) The reduction of the body surface area and the treatment-emergent adverse event rate had no statistically significant difference from the RLD (P &gt; 0.05). 5) The biosimilar CT-P43 and Bmab1200 demonstrated a lower probability of generating anti-drug antibodies, showing statistically significant differences from other biosimilars (P &lt; 0.05). Ustekinumab biosimilars demonstrate comparable efficacy and safety to ustekinumab-RP for treating moderate-to-severe PP in adults. The biosimilar CT-P43 is more effective in improving short-term PASI. Due to limitations in the number and quality of included studies, more high-quality studies are required to validate these findings.<p><a href="http://europepmc.org/article/MED/41957184?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">597</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>AR and ITGAL: Key Mediators of Andrographis paniculata's Anti-Psoriatic Effects Revealed by Multi-Omics Analysis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/ar-and-itgal-key-mediators-of-andrographis-paniculatas-anti-psoriatic-effects-revealed-by-multi-omics-analysis-r596/</link><description><![CDATA[<h4>Introduction</h4>This study analyzed the mechanisms of action of Andrographis paniculata (AP), a medicinal plant with diverse pharmacological properties, on psoriasis.<h4>Materials and methods</h4>The active components of AP and their corresponding targets were identified. These targets were subsequently intersected with differentially expressed genes (DEGs) and immune-related genes associated with psoriasis. The resulting gene set was subjected to functional enrichment analysis and immune infiltration analysis. The scRNA-seq data were analyzed to delineate the single-cell landscape in psoriasis and cell type-specific expression of genes of interest. Further, the molecular docking and experimental verification were performed for validation.<h4>Results</h4>Active components of AP and their targets were predicted. Cross-referencing these targets with psoriasis DEGs revealed 2 feature genes (AR and ITGAL), both exhibiting strong diagnostic potential. The two genes were associated with differentially enriched pathways and immune cell infiltration. Further, scRNA-seq analysis identified 10 cell subclusters. Notably, AR was expressed in reticular fibroblasts of healthy controls, while ITGAL was expressed in T cells of psoriasis samples. Molecular docking confirmed a stable binding interaction between Dehydroandrographolide and AR. In vitro validation using an M5 cytokine-induced keratinocyte model demonstrated that Dehydroandrographolide exerted potent anti-inflammatory and antiproliferative effects. Furthermore, it significantly modulated the protein expression levels of both genes.<h4>Discussion</h4>Combining in-silico and in-vitro analyses, this study identified AR and ITGAL as potential key mediators and validated the efficacy of the active component of AP, Dehydroandrographolide, against psoriasis.<h4>Conclusion</h4>Collectively, the study demonstrated that AP had the potential anti-psoriasis effects.<p><a href="http://europepmc.org/article/MED/41968824?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">596</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Analysis of Clinical Characteristics and Treatment Needs in Elderly Patients with Psoriasis Vulgaris: A Single-Centered Retrospective Study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/analysis-of-clinical-characteristics-and-treatment-needs-in-elderly-patients-with-psoriasis-vulgaris-a-single-centered-retrospective-study-r595/</link><description><![CDATA[<h4>Background</h4>Psoriasis is a chronic, immune-mediated skin disorder that causes physical, psychological, and social burdens. There is a growing need to better characterize the distinct clinical features and specific treatment needs of elderly patients with psoriasis, which remains an important area for further research to optimize care in this population.<h4>Objective</h4>To investigate the clinical characteristics, comorbidities, and treatment preferences of elderly patients with psoriasis vulgaris.<h4>Methods</h4>Patients with psoriasis vulgaris were included in this retrospective study. Data on demographics, disease characteristics, including age at diagnosis, body surface area (BSA), Psoriasis Area and Severity Index (PASI), Dermatology Life Quality Index (DLQI), comorbidities, and treatment needs were collected. Patients at the visit over 60 years of age were defined as elderly patients. Patients who were diagnosed before 40 years of age were defined as early-onset psoriasis (EOP), and patients who were diagnosed over 40 years of age were defined as late-onset psoriasis (LOP). Continuous variables were compared using t-tests or Mann-Whitney <i>U</i>-tests, categorical variables using Chi-square or Fisher's exact tests. Spearman correlation was used for association analysis. Statistical significance was set at <i>P</i>&lt;0.05.<h4>Results</h4>A total of 375 patients were included, comprising 70 (18.67%) elderly and 305 (81.33%) non-elderly patients. The elderly group had a significantly higher proportion of LOP (87.14% vs 48.76%, <i>P</i>&lt;0.05). A higher percentage of elderly patients had moderate-to-severe (27.14% vs 20.98%, <i>P</i>&lt;0.05) and severe (1.43% vs 0.66%, <i>P</i>&lt;0.05) disease. Comorbidities were more prevalent in the elderly, including cardiovascular disease (12.86% vs 3.93%, <i>P</i>&lt;0.05) and diabetes (12.86% vs. 1.31%, <i>P</i>&lt;0.05). Despite this, elderly patients reported lower DLQI scores (median 2.00 vs. 3.00, <i>P</i>&lt;0.05). Regarding treatment needs, elderly patients were less likely to prioritize reducing treatment costs (10.00% vs 20.98%, <i>P</i>&lt;0.05) and preventing disease recurrence (30.00% vs 44.26%,<i> P</i>&lt;0.05) compared to non-elderly patients. Within the elderly cohort, EOP patients exhibited more severe disease (median BSA: 3.00 vs 2.00; median PASI: 3.30 vs 0.80, <i>P</i>&lt;0.05), a higher rate of familial psoriasis (33.33% vs 4.92%, <i>P</i>&lt;0.05), and a greater demand for reducing treatment costs (33.3% vs 6.56%, <i>P</i>&lt;0.05) compared to LOP patients.<h4>Conclusion</h4>Elderly patients with psoriasis present a distinct clinical profile characterized by a high prevalence of late-onset disease, a significant comorbidity burden, and differing treatment priorities focused less on cost and recurrence. Despite the increased clinical severity, their perceived quality-of-life impact is lower. Besides, they report higher dissatisfaction linked to unmet needs in itch relief, drug safety, and long-term control. Within the elderly cohort, early-onset patients had more severe disease, stronger familial predisposition, and greater cost-related concerns. The findings highlight the necessity for age-specific, multidimensional management strategies for this population.<p><a href="http://europepmc.org/article/MED/41971650?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">595</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Associations between lifestyle factors and life quality in people living with psoriasis: results of the Asking People with Psoriasis about Lifestyle and Eating (APPLE) cross-sectional study.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/associations-between-lifestyle-factors-and-life-quality-in-people-living-with-psoriasis-results-of-the-asking-people-with-psoriasis-about-lifestyle-and-eating-apple-cross-sectional-study-r594/</link><description><![CDATA[<h4>Background</h4>Lifestyle factors have the potential to enhance well-being and quality of life (QoL). This study aimed to identify lifestyle patterns among UK-based adults with psoriasis and examine associations with QoL.<h4>Methods</h4>This was a cross-sectional analysis of the 'Asking People with Psoriasis about Lifestyle and Eating' (APPLE) study (n=353). QoL, Body Mass Index (BMI), and physical activity were assessed using the Dermatology Life Quality Index (DLQI), self-reported weight and height, and the International Physical Activity Questionnaire.<h4>Results</h4>Participant demography was: 82% female; mean (SD) age of 41 (13) years; and BMI of 27 (7) kg/m2. When fully adjusted for age, sex, smoking, and alcohol use, compared to individuals in the highest BMI tertile (35 (5) kg/m2), those in the lowest tertile (21 (2) kg/m2) reported a 71% reduced likelihood of QoL impairments (Odds Ratio (OR) = 0.29; 95% CI 0.14-0.59, adjusted P&lt;0.01). Dairy-free, gluten-free, and pescatarian diets were more frequently adopted in individuals reporting healthy BMIs (≈24 kg/m2, adjusted P&lt;0.05). Higher levels of physical activity (2932 (1509) Metabolic Equivalent of Task Minutes per week), and adequate sleep duration (7 (0) hours/day) were associated with lower odds of QoL impairments, although attenuated by multiple testing. Participants affected by embarrassment or self-consciousness related to their psoriasis engaged in less vigorous-intensity and walking activities compared to those who were less affected (adjusted P&lt;0.05).<h4>Conclusions</h4>Assessing weight status and physical activity in individuals reporting high DLQI scores may help identify modifiable behaviours contributing to poorer QoL and thereby shape interventions.<p><a href="http://europepmc.org/article/MED/41965125?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">594</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Development and validation of a prediction model for the risk of relapse in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/development-and-validation-of-a-prediction-model-for-the-risk-of-relapse-in-psoriasis-r593/</link><description><![CDATA[This study collected and analyzed clinical data of psoriasis patients to develop and validate a psoriasis relapse risk prediction model. It aims to support early relapse risk assessment in clinical practice and inform the design of preventive interventions. To develop and validate a risk prediction model for psoriasis relapse. A convenience sampling method was used to select 504 psoriasis patients admitted to a tertiary hospital in China between January 2022 and December 2024, including 353 cases in the training set and 151 cases in the testing set. Independent risk factors for psoriasis relapse were identified through univariate analysis and logistic regression analysis to develop a prediction model. A nomogram and SHAP summary plot were generated for model visualization, and the model's goodness of fit and discriminative ability were evaluated. The 1-year relapse rate of psoriasis patients after treatment was 66.67%. Logistic regression identified six independent risk factors for psoriasis relapse: BMI, diabetes, biologic use, smoking, upper respiratory tract infection (URTI), and non-standard medication, all of which were incorporated into the model. The area under the ROC curve (AUC) values for the training and testing sets were 0.767 [95% CI 0.715-0.818] and 0.704 [95% CI 0.620-0.789], respectively. The model showed moderate discrimination and good calibration. Decision curve analysis (DCA) confirmed clinically meaningful net benefit in both training and test sets. The predictive model for psoriasis relapse risk established in this study demonstrated only moderate predictive performance. This model can serve as a preliminary exploratory tool, providing a certain degree of quantitative reference for assessing the risk of psoriasis relapse; however, rigorous external validation in independent multicenter cohorts is still required before clinical application.<p><a href="http://europepmc.org/article/MED/41965844?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">593</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Atlantoaxial instability in psoriatic arthritis: Frequency and correlated factors from a single-center cohort.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/atlantoaxial-instability-in-psoriatic-arthritis-frequency-and-correlated-factors-from-a-single-center-cohort-r592/</link><description><![CDATA[<h4>Objectives</h4>There is very limited data regarding atlantoaxial instability (AAI) in patients with psoriatic arthritis (axPsA). In this study, we aimed to contribute to the existing literature on this topic.<h4>Methods</h4>Adult patients were included in this single-center study who were classified as PsA by the 'CASPAR' criteria and evaluated as having axial involvement according to the 'Calin' criteria. Those with inflammatory or non-inflammatory diseases that could affect the spine were excluded. Electronic patient files were reviewed retrospectively. Lateral neutral/full extension/full flexion and open-mouth anteroposterior cervical radiographs were evaluated by three rheumatologists blinded to the patients. Patients were compared in two groups as AAI-positive and AAI-negative.<h4>Results</h4>A total of 100 patients with a mean age of 48.8 years and a mean PsA duration of 7.4 years, 57% of whom were female, were included in the study. A total of 20 AAI lesions were detected in 18% patients; subaxial subluxation was detected in eight, anterior atlantoaxial subluxation (AAS) in seven, posterior AAS in three, lateral AAS in one, and vertical subluxation in one case. In the group with AAI, the presence of psoriasis (Ps) (p = 0.037), scalp psoriasis (p &lt; 0.001), and the use of targeted therapy for Ps and PsA (p &lt; 0.001, p &lt; 0.001) were significantly higher than in the AAI-negative group.<h4>Conclusion</h4>Given that Ps and PsA patients on targeted therapy may reflect cases with higher disease activity and inadequate response to conventional treatments, it may be appropriate to consider closer monitoring for AAI in these patients. Key Points • Atlantoaxial instability is present in approximately one-fifth of patients with axial psoriatic arthritis. • The most common instability lesion is subaxial subluxation, accounting for 40% of all lesions. • The presence of psoriasis, scalp psoriasis, and the use of targeted therapies for psoriatic arthritis or psoriasis are significantly more frequent in the group with atlantoaxial instability. These factors may be useful for cervical spine monitoring in patients with axial psoriatic arthritis. • The use of targeted therapies for psoriatic arthritis or psoriasis may indirectly indicate an association between high disease activity and atlantoaxial instability.<p><a href="http://europepmc.org/article/MED/41973139?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">592</guid><pubDate>Tue, 14 Apr 2026 07:32:37 +0000</pubDate></item><item><title>Alox8 knockout exacerbates imiquimod-induced psoriasis-like inflammation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/alox8-knockout-exacerbates-imiquimod-induced-psoriasis-like-inflammation-r591/</link><description><![CDATA[Lipoxygenases peroxidise polyunsaturated fatty acids, resulting in oxylipins, which may act pro- or anti-inflammatory. Arachidonate 15-lipoxygenase type B was shown to play a role in the resolution of keratinocyte inflammation and is upregulated in psoriasis. Its murine ortholog, arachidonate 8-lipoxygenase (Alox8), differs in regiospecificity in that it adds molecular oxygen to the 8th and not 15th carbon of arachidonic acid. This study aimed to determine if Alox8 plays a role in the resolution of murine imiquimod-induced psoriasis. Alox8 knockout (KO) mice, which are not commercially available, were generated with a functional KO targeting the enzyme's active site. Untargeted Lipidomics revealed changes in the skin lipidome from both imiquimod-induced psoriasis as well as between wild-type and KO mice. Furthermore, LC-MS/MS revealed a functional KO with reductions in Alox8-specific oxylipins. Lipid peroxidation marker 4-hydroxynonenal was elevated in the epidermis of wild-type mice from imiquimod treatment, however, it was significantly reduced in Alox8 KO mice. Alox8 KO mice exhibited a thickened epidermis, resulting from reduced DNA damage and increased proliferation. Moreover, immune cell infiltration was enhanced in Alox8 KO mice, including a higher abundance of γδ T cells. Elevated cytokine levels of interleukin-17 and -22, accompanied by keratinocyte-produced C-X-C motif chemokine ligand 1, were detected in the skin of Alox8 KO mice. Additionally, cyclooxygenase 2 expression and prostaglandin E<sub>2</sub> levels were enhanced in Alox8 KO mice. These data demonstrate an exacerbated and prolonged inflammatory psoriasis phenotype in Alox8 KO mice, implying that Alox8 aids in the resolution of murine psoriasis.<p><a href="http://europepmc.org/article/MED/41963292?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">591</guid><pubDate>Mon, 13 Apr 2026 09:49:58 +0000</pubDate></item><item><title>Systemic Inflammatory Indexes as Easy-to-Use Markers for Monitoring Psoriasis and Hidradenitis Suppurativa.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/systemic-inflammatory-indexes-as-easy-to-use-markers-for-monitoring-psoriasis-and-hidradenitis-suppurativa-r590/</link><description><![CDATA[<small>No abstract supplied.</small><p><a href="http://europepmc.org/article/MED/41954307?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">590</guid><pubDate>Mon, 13 Apr 2026 09:49:58 +0000</pubDate></item><item><title>Effects of biologics and small-molecule inhibitors on lipid profiles in patients with psoriasis or psoriatic arthritis: An analysis of current evidence.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/effects-of-biologics-and-small-molecule-inhibitors-on-lipid-profiles-in-patients-with-psoriasis-or-psoriatic-arthritis-an-analysis-of-current-evidence-r589/</link><description><![CDATA[<h4>Importance</h4>Available evidence reveals markedly divergent metabolic signatures across biologics and small-molecule inhibitors, highlighting the need for further investigations.<h4>Objective</h4>To address this knowledge gap, we performed a systematic review and meta-analysis of randomized controlled trials (RCTs) and observational studies in patients with psoriasis or psoriatic arthritis (PsA) to quantify the short- and long-term effects of targeted therapies on lipid profiles.<h4>Evidence review</h4>PubMed, Embase, and Cochrane databases were searched for RCTs and observational studies published through July 25, 2025. Eligible randomized RCTs were evaluated using the Cochrane Risk of Bias tool, while nonrandomized studies were assessed using the Methodological Index for Non-Randomized Studies. All lipid effect estimates were derived from within-group pre-to-post changes in patients with psoriasis or PsA.<h4>Findings</h4>Thirty-six articles involving 21,477 patients with psoriasis and 3098 patients with PsA (total 24,575) across seven targets were analyzed. The long-term use of Janus kinase inhibitors (JAKi) significantly increases total cholesterol (TC; weighted mean difference [WMD] = 7.03; 95% confidence interval [CI] = 1.22, 12.84), triglyceride (TG; WMD = 19.98; 95% CI = 13.82, 26.14), high-density lipoprotein cholesterol (HDL-c; WMD = 6.87; 95% CI = 4.38, 9.36), and low-density lipoprotein cholesterol (LDL-c; WMD = 12.37; 95% CI = 7.24, 17.50) levels. Long-term tumor necrosis factor alpha inhibitors (TNFi) significantly lowers TC (WMD = -8.40; 95% CI = -15.21, -1.60), TG (WMD = -15.22; 95% CI = -21.92, -8.51), and LDL-c (WMD = -10.61; 95% CI = -16.77, -4.45) levels while raising HDL-c (WMD = 4.13; 95% CI = 1.23; 7.03) levels. Long-term interleukin-17 A inhibitors significantly increases TG (WMD = 7.31; 95% CI = 3.17, 11.46) levels, whereas IL-23p19 inhibitors yield the opposite effect (WMD = -32.08; 95% CI = -51.87, -12.30).<h4>Conclusions and relevance</h4>Our data underscore the need for routine lipid monitoring during TNF-α- and JAK-targeted therapy in patients with psoriasis or PsA. Due to the limitations of our analysis, well-designed prospective trials with extended follow-up periods are warranted to validate and refine these observations.<p><a href="http://europepmc.org/article/MED/41935726?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">589</guid><pubDate>Sat, 11 Apr 2026 17:37:02 +0000</pubDate></item><item><title>Dimethyl fumarate attenuates subcutaneous adipose tissue inflammation in psoriasis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/dimethyl-fumarate-attenuates-subcutaneous-adipose-tissue-inflammation-in-psoriasis-r588/</link><description><![CDATA[Psoriasis is a chronic immune-mediated inflammatory disease with systemic manifestations beyond the skin, yet the role of subcutaneous adipose tissue (SAT) in disease biology and therapeutic response remains poorly understood. Here, we investigated inflammatory features of SAT in psoriasis and the effects of dimethyl fumarate (DMF) on this compartment. Six adults with moderate-to-severe plaque psoriasis received oral DMF for 24 weeks and were clinically evaluated measuring the Psoriasis Area and Severity Index (PASI), showing a consistent reduction in disease severity during treatment. Publicly available spatial transcriptomic data were analysed to profile inflammatory signatures in SAT clusters of psoriatic versus healthy skin. Bulk RNA sequencing was performed on SAT biopsies obtained from psoriatic plaques before and after DMF treatment in four patients. Complementary in vitro models using murine 3T3-L1 adipocytes and human adipocytes differentiated from mesenchymal stem cells were exposed to pro-inflammatory cytokines or macrophage-conditioned media (CM) with or without DMF to assess effects on inflammatory gene expression and NF-κB signalling. Spatial transcriptomics identified enrichment of inflammation-related pathways in SAT beneath psoriatic lesions. DMF treatment was associated with reduced expression of inflammatory mediators and with a shift in SAT transcriptional profile toward patterns observed in healthy tissue. In vitro, DMF significantly attenuated cytokine- and CM-induced adipocyte activation and reduced NF-κB phosphorylation in both murine and human adipocyte models. These data provide integrated clinical and experimental evidence that DMF treatment is associated with reduced disease activity and attenuation of inflammatory signalling within psoriatic SAT, supporting adipose tissue as a potentially modifiable inflammatory compartment in psoriasis.<p><a href="http://europepmc.org/article/MED/41962229?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">588</guid><pubDate>Sat, 11 Apr 2026 17:37:02 +0000</pubDate></item><item><title>Alox8 knockout exacerbates imiquimod-induced psoriasis-like inflammation.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/alox8-knockout-exacerbates-imiquimod-induced-psoriasis-like-inflammation-r587/</link><description><![CDATA[Lipoxygenases peroxidise polyunsaturated fatty acids, resulting in oxylipins, which may act pro- or anti-inflammatory. Arachidonate 15-lipoxygenase type B was shown to play a role in the resolution of keratinocyte inflammation and is upregulated in psoriasis. Its murine ortholog, arachidonate 8-lipoxygenase (Alox8), differs in regiospecificity in that it adds molecular oxygen to the 8th and not 15th carbon of arachidonic acid. This study aimed to determine if Alox8 plays a role in the resolution of murine imiquimod-induced psoriasis. Alox8 knockout (KO) mice, which are not commercially available, were generated with a functional KO targeting the enzyme's active site. Untargeted Lipidomics revealed changes in the skin lipidome from both imiquimod-induced psoriasis as well as between wild-type and KO mice. Furthermore, LC-MS/MS revealed a functional KO with reductions in Alox8-specific oxylipins. Lipid peroxidation marker 4-hydroxynonenal was elevated in the epidermis of wild-type mice from imiquimod treatment, however, it was significantly reduced in Alox8 KO mice. Alox8 KO mice exhibited a thickened epidermis, resulting from reduced DNA damage and increased proliferation. Moreover, immune cell infiltration was enhanced in Alox8 KO mice, including a higher abundance of γδ T cells. Elevated cytokine levels of interleukin-17 and -22, accompanied by keratinocyte-produced C-X-C motif chemokine ligand 1, were detected in the skin of Alox8 KO mice. Additionally, cyclooxygenase 2 expression and prostaglandin E2 levels were enhanced in Alox8 KO mice. These data demonstrate an exacerbated and prolonged inflammatory psoriasis phenotype in Alox8 KO mice, implying that Alox8 aids in the resolution of murine psoriasis.<p><a href="http://europepmc.org/article/MED/41963292?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">587</guid><pubDate>Sat, 11 Apr 2026 17:37:02 +0000</pubDate></item><item><title>Impact of Pediatric Psoriasis on Child and Caregiver Health-Related Quality of Life: A Systematic Review and Meta-Analysis.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/impact-of-pediatric-psoriasis-on-child-and-caregiver-health-related-quality-of-life-a-systematic-review-and-meta-analysis-r586/</link><description><![CDATA[<h4>Background</h4>Pediatric psoriasis is a chronic inflammatory skin disease that affects both physical and psychosocial well-being. The impact of the disease extends beyond the patient, significantly affecting caregivers' emotional and functional quality of life.<h4>Objectives</h4>This systematic review and meta-analysis aimed to evaluate the health-related quality of life (HrQOL) burden of pediatric psoriasis on children and their caregivers. The study also sought to identify clinical and child-related factors associated with increased impairment in HrQOL.<h4>Methods</h4>A systematic search of MEDLINE and Embase databases was conducted according to PRISMA guidelines. Studies included children under 18 years of age with a diagnosis of psoriasis and/or their caregivers, reporting outcomes using validated HrQOL measures. Two reviewers independently screened studies, extracted data, and assessed quality using the Mixed Methods Appraisal Tool. Where appropriate, correlation coefficients were pooled using random-effects meta-analysis after Fisher's Z-transformation.<h4>Results</h4>Twenty-one studies were included, encompassing 1038 children and 1161 caregivers. The most commonly used instruments were the Children's Dermatology Life Quality Index (CDLQI) and Family Dermatology Life Quality Index (FDLQI). Across studies, 84.8% of children and 96.1% of caregivers experienced some degree of HrQOL impairment. Meta-analysis revealed a moderate positive correlation between child disease severity (PASI scores) and caregiver HrQOL burden (r = 0.463), while no significant correlation was found with child age or disease duration. Amongst children, HrQOL was most affected in the domains of symptoms, leisure, and treatment-related concerns.<h4>Conclusions</h4>Pediatric psoriasis exerts a substantial impact on both child and caregiver quality of life, with greater burden associated with more severe disease. These findings highlight the need for early intervention and psychosocial support targeting families. Clinicians should consider the broader family context when managing pediatric psoriasis and prioritize counseling during disease flares to mitigate emotional and functional strain.<p><a href="http://europepmc.org/article/MED/41960930?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">586</guid><pubDate>Sat, 11 Apr 2026 17:37:02 +0000</pubDate></item><item><title>Targeting TYK2 in Cutaneous Autoimmunity: Deucravacitinib-Induced Remission of Discoid Lupus and Psoriasis with Supportive Confocal Microscopy Findings.</title><link>https://www.psoriasis-news.de/articles.html/1_articles/targeting-tyk2-in-cutaneous-autoimmunity-deucravacitinib-induced-remission-of-discoid-lupus-and-psoriasis-with-supportive-confocal-microscopy-findings-r585/</link><description><![CDATA[<h4>Introduction</h4>Cutaneous lupus erythematosus (CLE), particularly discoid lupus erythematosus (DLE), is a chronic autoimmune condition driven in part by type I interferon signaling. No systemic therapies are specifically approved for CLE, and management is often extrapolated from systemic lupus erythematosus. Deucravacitinib, a selective oral tyrosine kinase 2 (TYK2) inhibitor targeting the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, has shown efficacy in psoriasis and emerging promise in lupus.<h4>Case report</h4>We describe a 29-year-old woman with biopsy-proven DLE refractory to prednisone and hydroxychloroquine who subsequently developed moderate-to-severe plaque psoriasis (Psoriasis Area and Severity Index [PASI] 16). Initial treatment with ixekizumab improved psoriasis but failed to control DLE, and psoriatic lesions later relapsed. Therapy was switched to deucravacitinib 6 mg daily. After 9 weeks, marked improvement of both conditions was observed (PASI 0.2) with progressive regression of DLE lesions. By week 27, complete clinical remission of psoriasis (PASI 0) and full resolution of DLE lesions were achieved, confirmed by reflectance confocal microscopy.<h4>Conclusion</h4>This case highlights the potential of deucravacitinib as an effective therapeutic option for refractory DLE, particularly in patients with concomitant psoriasis, supporting TYK2 inhibition as a promising targeted strategy in cutaneous autoimmunity.<p><a href="http://europepmc.org/article/MED/41957317?source=rss" rel="external nofollow">Weiterlesen</a></p>]]></description><guid isPermaLink="false">585</guid><pubDate>Sat, 11 Apr 2026 17:37:02 +0000</pubDate></item></channel></rss>
