Experimental Dermatology最新文献

{"title":"Aquaporin 3 Promoter Polymorphisms Reduce Gene Expression and Associate Altered Autophagy-Related Gene Signatures With Atopic Dermatitis Susceptibility","authors":"Yi Ying Eliza Lim,&nbsp;Yang Yie Sio,&nbsp;Terence Yin Weng Lam,&nbsp;Yee-How Say,&nbsp;Kavita Reginald,&nbsp;Fook Tim Chew","doi":"10.1111/exd.70358","DOIUrl":"10.1111/exd.70358","url":null,"abstract":"<p>Genome-wide association studies (GWAS) have uncovered multiple loci associated with atopic dermatitis (AD), although mechanistic understanding remains limited. Here, we examine a risk variant in the <i>aquaporin 3</i> (<i>AQP3</i>) promoter and propose a mechanistic link between genotype to altered autophagy, skin barrier integrity, and wound healing in AD. A GWAS involving 1261 AD cases and 4062 controls of Chinese ancestry from the Singapore–Malaysia cohort was performed. Linkage disequilibrium (LD) analysis and cis-eQTL datasets were used to assess regulatory associations. Functional effects of promoter variants were validated using in vitro luciferase assays and ex vivo transcriptomic profiling. In vitro experiments in HaCaT keratinocytes investigated the effect of siRNA-mediated <i>AQP3</i> knockdown on autophagy, skin barrier integrity, and wound closure. A discovery GWAS identified significant association between AD and SNP rs12555686 (<i>p</i> = 1.67 × 10⁻¹¹, OR = 1.89), located in the promoter of <i>AQP3</i>. Two additional SNPs in strong LD (rs2231225, rs3758279) formed a major haplotype associated with reduced <i>AQP3</i> expression. Reduced <i>AQP3</i> expression was associated with decreased autophagy markers (<i>Beclin1</i>, <i>ATG5</i>, <i>ATG12</i>, <i>GABARAPL2, LAMP2, ATG4C</i>), increased senescence markers (<i>p21</i>, <i>GADD45A</i>, <i>SERPINE1</i>), and elevated inflammatory cytokines (<i>IL8</i>, <i>IL1B</i>, <i>TNF</i>). Lastly, <i>AQP3</i> knockdown in HaCaT keratinocytes reduced steady-state LC3B-II/LC3B-I ratio, reduced occludin expression, and delayed wound healing in vitro. Promoter variants in <i>AQP3</i> link genetic susceptibility to gene signatures consistent with altered autophagy, cellular senescence, and inflammation in AD. These findings highlight <i>AQP3</i> as a potential modulator of both epithelial and immune-related mechanisms in AD pathogenesis.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13577822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Antimicrobial Peptides of the Skin: Roles in Skin Cancer and Clinical Applications’","authors":"","doi":"10.1111/exd.70359","DOIUrl":"10.1111/exd.70359","url":null,"abstract":"<p>\u0000 <span>E. Botto</span>, <span>Z. M. Lipman</span>, <span>L. A. Temiz</span>, <span>L. Correa-Selm</span>, and <span>J. M. Grichnik</span>, “ <span>Antimicrobial Peptides of the Skin: Roles in Skin Cancer and Clinical Applications</span>,” <i>Experimental Dermatology</i> <span>35</span>, no. <span>8</span> (<span>2026</span>): e70341, https://doi.org/10.1111/exd.70341.\u0000 </p><p>The name of the fourth author ‘Lilia Corea-Selm’ was misspelled and has been updated to ‘Lilia Correa-Selm’.</p><p>The online version of this article has been corrected accordingly.</p><p>We apologize for this error.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/exd.70359","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Future Integration of Biomarkers for Inflammatory Skin Diseases Into Daily Practice: A Survey Among a Multifaceted Group of Patients and Dermatological Care Providers","authors":"Linda T. H. Godding,&nbsp;Elke M. G. J. de Jong,&nbsp;Sylvia van Beugen,&nbsp;Antoinette I. M. van Laarhoven,&nbsp;Els van der Pool,&nbsp;Nanda J. Olde,&nbsp;Debra Trampe,&nbsp;Hanna Niehues,&nbsp;Ilse van Ee,&nbsp;Annemarie Sluijmers,&nbsp;Robert Rissmann,&nbsp;Juul M. P. A. van den Reek,&nbsp;Marieke M. B. Seyger,&nbsp;the Next Generation ImmunoDermatology Consortium (NGID)","doi":"10.1111/exd.70352","DOIUrl":"10.1111/exd.70352","url":null,"abstract":"<p>Successful implementation of dermatological biomarkers depends on early understanding of clinical needs and adoption barriers. Yet, research on these factors as perceived by dermatological care providers (DCPs) is scarce and perspectives of patients are largely underexplored. This survey study among patients and DCPs assessed biomarker needs and adoption barriers and facilitators for five inflammatory skin diseases: psoriasis (PsO), atopic dermatitis (AD), hidradenitis suppurativa (HS), cutaneous lupus erythematosus (CLE) and chronic spontaneous urticaria (CSU). In total, the study population consisted of 591 patients and 99 DCPs. Across all skin diseases, both groups mainly prioritized a biomarker for prediction of therapeutic response, however, DCPs prioritized this substantially more often than patients, especially for PsO (79.8% vs. 31.3% resp.), AD (68.7% vs. 37.1% resp.) and HS (66.7% vs. 34.4% resp.). Notably, a biomarker for the prediction of the risk to develop comorbidities was prioritized relatively often by patients (7.0%–19.4%), whereas DCPs only substantially prioritized this for CLE (14.1%). To enhance implementation, patients must ideally be able to undergo biomarker collection nearby their homes (travel time &lt; 1 h) with complete reimbursement. For DCPs it is important that the biomarker is well validated, non-invasive and measurable during regular visits with preferably a short sampling time.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AI-Based Segmentation of Wound Types Caused by Epidermolysis Bullosa","authors":"Georg Wimmer,&nbsp;Christian Puttinger,&nbsp;Pamina Schlager,&nbsp;Roland Zauner,&nbsp;Carolin Gemeier,&nbsp;Tobias Welponer,&nbsp;Christine Prodinger,&nbsp;Anja Diem,&nbsp;Katharina Ude-Schoder,&nbsp;Christina Guttmann-Gruber,&nbsp;Bernadette Liemberger,&nbsp;Martin Laimer,&nbsp;Johann W. Bauer,&nbsp;Andreas Uhl","doi":"10.1111/exd.70356","DOIUrl":"10.1111/exd.70356","url":null,"abstract":"<p>Epidermolysis bullosa (EB) defines a group of rare, inherited and currently incurable genetic disorders characterized by excessive skin fragility, with blistering and wounding of skin and mucous membranes upon minor mechanical trauma. Accurate wound assessment is imperative for measuring and longitudinal monitoring of disease activity and for determining the most accurate treatment. In this work, we describe the annotation of clinical images from EB patients and the subsequent training of both classical convolutional neural networks and state-of-the-art transformer-based architectures for the segmentation of various categories of EB skin wounds. Utilising our dataset of 260 EB images from 18 patients and the corresponding 536 expert-annotated segmentation masks, we train and evaluate five different model architectures and compare their performance against human inter-annotator agreement. External evaluation was not possible because no comparable annotated EB datasets are available. Our results demonstrate that transformer-based models, particularly Mask2Former, achieve near-expert-level segmentation accuracy in five of the seven categories and even surpass human inter-annotator agreement in two. Models based on convolutional neural networks perform noticeably worse and generally fail to accurately segment rarely occurring classes. Averaged over all categories, Mask2Former achieved a mean dice similarity coefficient (DSC) of 52.9%, compared to an inter-annotator agreement of 55.9%. These results indicate that Mask2Former has the potential to serve as a clinical decision support system to improve wound segmentation and categorization. Furthermore, this model provides a foundation for planned future applications in automated wound measurement, wound progression monitoring and documentation and the development of a smartphone-based telemedicine application.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicastrin Regulates Cutaneous Squamous Cell Carcinoma Progression Through the MAPK/ERK Signalling","authors":"Shumeng Xue,&nbsp;Yuanxing Shen,&nbsp;Chong Zhang,&nbsp;Qian Ye,&nbsp;Yi Zhang,&nbsp;Haoxiang Xu,&nbsp;Yanyan He","doi":"10.1111/exd.70350","DOIUrl":"10.1111/exd.70350","url":null,"abstract":"<div>\u0000 \u0000 <p>Cutaneous squamous cell carcinoma (cSCC) is among the most common epithelial malignancies. Although cSCC arising in long-standing acne inversa (AI) lesions is rare, it is a severe and clinically important complication of AI. Approximately one-third of patients with AI harbour loss-of-function mutations in <i>NCSTN</i>. Whether NCSTN loss contributes to cSCC development remains unclear. To address this, we first examined its expression pattern in cSCC tissues. Interestingly, NCSTN expression was significantly decreased in cSCC tissues by immunohistochemistry (IHC) and Western blotting. Furthermore, loss of NCSTN promoted cSCC cell proliferation and migration in vitro and tumour growth in vivo. Proteomic analysis revealed that NCSTN deficiency promoted cell proliferation through activation of the MAPK/ERK signalling pathway, accompanied by reduced CLDN3 expression and alterations in cell-adhesion-related pathways. To validate the functional relevance of this signalling axis in vivo, we treated NCSTN-knockdown tumour-bearing mice with the ERK inhibitor SCH772984, which effectively suppressed tumour growth. Collectively, these findings demonstrate that loss of NCSTN drives cSCC progression through activation of MAPK/ERK signalling, and identify ERK signalling as a potential therapeutic vulnerability in NCSTN-deficient cSCC.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Umbilical Cord-Derived Therapies for Wound Healing: A Scoping Review of Clinical and Translational Evidence","authors":"Juling Sia,&nbsp;Sandy Chua,&nbsp;Akimichi Morita,&nbsp;Bernett Lee,&nbsp;Hazel H. Oon","doi":"10.1111/exd.70353","DOIUrl":"10.1111/exd.70353","url":null,"abstract":"<p>Wound healing is a complex process, and although there are existing wound management therapies, they can be limited by poor response rate, cosmetic concerns and other procedure-related risks. Umbilical cord (UC) and umbilical cord blood (UCB)-based therapies have therefore emerged as an area of research interest that aims to address current limitations in wound management. This scoping review summarises the extent of research into these therapies, including mechanisms of action, clinical translation and artificial modifications. A systematic search of two electronic databases (PubMed and Embase-Ovid) was carried out before supplementation with reference list screening and citation tracking. Of the 133 included articles, there were 20 in vitro studies, 19 review articles, 1 editorial, 16 human studies and 77 animal studies. UC and UCB-based therapies consist of cellular and acellular factors that act through paracrine mechanisms rather than direct differentiation. Immunomodulation, growth stimulation, angiogenesis and anti-apoptosis are the main mechanisms by which these therapies exert their effect, and initial reports provide some evidence that these therapies could be useful clinically. Nevertheless, such preliminary evidence is limited by study heterogeneity, short follow-up durations and small sample sizes. Various modifications to these therapies, such as preconditioning, are also being explored to increase treatment yield. Although infection and multi-organ effects are common safety concerns, current literature has also yet to establish long-term safety. Preclinical data on UC-based therapies appear promising; however, larger multicentric human trials are essential to validate clinical efficacy. Furthermore, comprehensive evaluations of safety and standardisation protocols will be critical for clinical translation.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13547771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COCH Expression in the Hair Follicle Microenvironment Is Associated With Cortical Disulfide Bonding and Tensile Resistance in Aging Hair","authors":"Hyun Woo Joo,&nbsp;Gyusang Jeong,&nbsp;Seung Hyun Shin,&nbsp;Su Na Kim,&nbsp;Donghyun Kim,&nbsp;Mira Ham,&nbsp;Hyoung-June Kim,&nbsp;Byung Cheol Park,&nbsp;Won-Seok Park,&nbsp;Incheol Seo,&nbsp;Young Kwan Sung","doi":"10.1111/exd.70348","DOIUrl":"10.1111/exd.70348","url":null,"abstract":"<p>Although hair aging affects appearance and hair quality, objective biomarkers linking molecular alterations to clinically relevant mechanical properties of hair remain limited. Here, we investigated the relationships among age, hair tensile resistance, and cortical disulfide bond content. Hair shafts from healthy volunteers (20–40 years vs. &gt; 50 years) were analysed for tensile resistance, which was measured as maximum tensile force, and disulfide bond content was assessed by Raman spectroscopy. In parallel, human scalp hair follicles were stratified according to disulfide bond content and donor age to generate transcriptomic datasets for analysis. We identified follicular gene-expression signatures associated with these parameters. Differential expression analysis revealed a shared gene set associated with reduced disulfide bond content and age, which was subsequently evaluated in ex vivo human hair follicle cultures. Among these candidates, cochlin (<i>COCH</i>) emerged as a prominent candidate gene associated with higher cortical disulfide bond content and enhanced tensile resistance of the hair shaft. Immunohistochemical analysis revealed that COCH predominantly localized to the hair matrix and outer root sheath, supporting a follicle-derived contribution to shaft biochemistry. Together, these findings identify COCH as a promising candidate marker linked to disulfide bond integrity and tensile properties of human hair and establish an integrative framework for connecting follicular gene expression with age-associated changes in hair shaft mechanics.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein Post-Translational Modifications in UV-Induced Skin Damage","authors":"Yuanyuan Xu,&nbsp;Chong Zhang,&nbsp;Tianyi Zhang,&nbsp;Yan Yan,&nbsp;Baoxi Wang","doi":"10.1111/exd.70326","DOIUrl":"10.1111/exd.70326","url":null,"abstract":"<p>Ultraviolet (UV) irradiation leads to acute photodamage, photoaging and skin cancers. Post-translational modifications (PTMs) represent a key regulatory layer by modulating protein function, localization and interactions under UV stress. This review discusses the mechanistic involvement of PTMs in UV-induced skin damage and summarizes emerging PTM-related photoprotective strategies. Phosphorylation is a central mediator of UV-induced signal transduction, driving activation of the epidermal growth factor receptor (EGFR) and its downstream signalling pathways. Acetylation exerts distinct regulatory effects: histone acetylation primarily regulates transcription of inflammation-related genes and matrix metalloproteinases (MMPs), while non-histone acetylation modulates cellular senescence and mitochondrial antioxidant defence through modification of key proteins. Ubiquitination regulates protein degradation and, through non-degradative modifications, participates in DNA damage recognition and nucleotide excision repair (NER). Furthermore, other PTMs, including methylation, glycosylation, citrullination, SUMOylation and poly(ADP-ribosyl)ation (PARylation), participate in diverse regulatory processes during UV-induced cutaneous alterations. Experimental and emerging interventions associated with PTMs in UV-induced skin damage range from natural extracts to small-molecule agents and mainly include upstream-level modulation of oxidative stress, metabolic status or key effector protein function, as well as enzyme-level modulation of PTM writers and erasers. Different classes of PTMs contribute to UV-induced skin damage through distinct regulatory mechanisms. Further studies should explore the roles of emerging and less-characterized PTMs and evaluate interventions targeting PTM-regulating enzymes in physiologically relevant skin models.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13535276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DPP4 Substrate Supplementation Protects From WNT-Induced Lipid Depletion in Dermal Adipocytes","authors":"Suneeti R. Madhavan,&nbsp;Piper Moore,&nbsp;Qiannan Ma,&nbsp;Radhika P. Atit","doi":"10.1111/exd.70354","DOIUrl":"https://doi.org/10.1111/exd.70354","url":null,"abstract":"<div>\u0000 \u0000 <p>Adipocytes exhibit remarkable plasticity, dynamically gaining and losing lipid content. However, during skin fibrosis, this adaptability becomes detrimental as adipocytes undergo lipid depletion associated with disease pathology. We previously identified the WNT signalling pathway—acting through Dipeptidyl Peptidase IV (DPP4) – as a key mediator of lipid depletion associated with skin fibrosis, but the mechanism remains unclear. DPP4 is an exopeptidase that cleaves a wide array of substrates across different cell types. Here, we investigate whether modulation of lipid-regulating DPP4 substrates is sufficient to preserve lipid content in WNT-activated dermal adipocytes. Using two complementary strategies, we found that supplementation with the DPP4 substrates Neuropeptide Y (NPY) and Glucose-dependent Insulinotropic Peptide (GIP) can partially protect lipid content in dermal adipocytes. When used in combination, we found that the protection against lipid depletion was more effective than monotherapy alone. These findings demonstrate that supplementation with DPP4 substrates provides a basis for targeted treatments for lipodystrophy syndromes and skin fibrosis.</p>\u0000 </div>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148816486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Adverse Event Profile of Apremilast: Pharmacovigilance Study Based on FDA Adverse Event Reporting System (FAERS)’","authors":"","doi":"10.1111/exd.70351","DOIUrl":"10.1111/exd.70351","url":null,"abstract":"<p>\u0000 <span>K. Gan</span>, <span>J. Liu</span>, <span>J. Shen</span>, et al. “ <span>Adverse Event Profile of Apremilast: Pharmacovigilance Study Based on FDA Adverse Event Reporting System (FAERS)</span>,” <i>Experimental Dermatology</i> <span>35</span>, no. <span>7</span> (<span>2026</span>): e70303, https://doi.org/10.1111/exd.70303.\u0000 </p><p>In the above article, the equal contribution statement is currently published as:</p><p>‘Jie Liu contributed equally to this study’.</p><p>To meet the strict evaluation requirements of author's institution, this statement needs to be more specific to indicate exactly who contributed equally. This should be revised to:</p><p>‘Ke Gan and Jie Liu contributed equally to this work’.</p><p>The article category has been published as ‘Review Article’, which is incorrect. The correct article category is ‘Research Article’.</p><p>We apologize for the error.</p>","PeriodicalId":12243,"journal":{"name":"Experimental Dermatology","volume":"35 8","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}