EXPERIMENTAL DERMATOLOGY实验皮肤病学
EXPERIMENTAL DERMATOLOGY(英文缩写 EXP DERMATOL),ISSN 0906-6705,eISSN 1600-0625,中文译名:实验皮肤病学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.511 | Q1 |
| 2022 | 3.600 | Q1 |
| 2023 | 3.500 | Q1 |
| 2024 | 3.100 | Q2 |
| 2025 | 3.400 | Q2 |
EXPERIMENTAL DERMATOLOGY 最新收录文献
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1. {"_":"Selective Expansion of TCR Vβ2 Tregs and Impaired Lymphocyte TSST-1 Responsiveness in Bullous Pemphigoid Patients Colonised by Staphylococcus aureus.","sup":["+"]}
PMID:日期:2026-09-01Bullous pemphigoid (BP) is an autoimmune blistering disease of the elderly who are frequently colonised by Staphylococcus aureus, particularly strains producing the superantigen toxic shock syndrome toxin-1 (TSST-1). Given the ability of TSST-1 to engage the T cell receptor (TCR) Vβ2 chain, we investigated whether superantigen (SAg) exposure in BP is associated with alterations in peripheral T cell populations. CD4 T cells were isolated from peripheral blood mononuclear cells (PBMCs) from BP patients and age-matched healthy controls. T cell responsiveness to TSST-1, staphylococcus enterotoxin G (SEG), and staphylococcus enterotoxin-like-I (SEl-I) was assessed via proliferation assays, and the TCR Vβ repertoire was analysed by RT-qPCR of bulk CD4 T cells and flow cytometry of conventional CD4, CD8, and regulatory T cell (Treg, CD4FoxP3) subsets. Contrary to expectations, proliferative responses to TSST-1 were significantly lower in BP samples than in controls, while responses to SEG and SEl-I were comparable. RT-qPCR revealed no expansion of Vβ2 in bulk CD4 T cells, and surface phenotyping detected no enrichment of Vβ2 cells within conventional CD4 or CD8 T populations. In contrast, Vβ2 cells were selectively enriched within the Treg compartment. These findings indicate that peripheral T cell responses to TSST-1 are attenuated in BP and are associated with subset-specific skewing of the TCR repertoire. These findings are consistent with increased regulatory features in the peripheral immune compartment that may limit systemic SAg reactivity. Studies examining lesional skin immune populations are needed to determine whether local T cell responses differ from those observed in peripheral blood.
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3. Syk Inhibition Sensitizes Skin Squamous Carcinoma Cells to TRAIL-Induced Apoptosis.
PMID:日期:2026-09-01Spleen tyrosine kinase (Syk) regulates immune responses and has been implicated in haematopoietic and epithelial cancers. Although our previous studies showed that Syk modulates keratinocyte differentiation and UVB-induced inflammation, its role in UVB-related cutaneous squamous cell carcinoma (cSCC) remains unclear. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in cancer cells and is expressed in healthy skin but reduced in non-melanoma skin cancers and sun-exposed skin. This study investigated the role of Syk in cSCC and TRAIL-induced apoptosis. Immunohistochemistry revealed elevated phosphorylated and total Syk levels in SCC tissues compared with normal skin. In SCC12 cells, TRAIL induced dose-dependent apoptosis, which was enhanced by pharmacological Syk inhibition or Syk silencing. Combination treatment with TRAIL and Syk inhibitors increased annexin V positivity and cleavage of caspase-3, PARP1 and Bid, accompanied by reduced Mcl-1 expression. Mechanistically, TRAIL induced Src and Syk phosphorylation. TRAIL-induced Syk activation was suppressed by Src inhibition but not by EGFR inhibition, indicating that Syk activation is Src-dependent but EGFR-independent in this pathway. Syk inhibition further reduced TRAIL-activated Akt and MAPK signalling, while Akt activation may play a role in regulating SCC12 survival. These results suggest that targeting Syk sensitizes TRAIL-mediated apoptosis and may offer a promising therapeutic strategy for treating cutaneous SCC.
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4. Atopic Dermatitis, Sleep Quality, and Cognitive Difficulties in US Adults: A 2024 NHIS Mediation Analysis.
PMID:日期:2026-09-01该文献暂无摘要。
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5. Melasma: When Dermal Photoageing Precedes Melanocyte Ageing.
PMID:日期:2026-09-01Melasma is a chronic relapsing hyperpigmentary disorder with difficult long-term management. In this review, melasma is proposed as a disorder of persistent melanocyte activation sustained within a photoaged dermal microenvironment. This microenvironment, composed of senescent fibroblasts, UV-activated sebocytes and vascular components, functions as a dermal melanogenic field that continuously provides melanogenic signalling. We further propose that melasma may arise within a melanogenic window, a phase characterized by a photoaged dermis and melanocytes that remain responsive to melanogenic stimulation. This window may result from dermal ageing preceding melanocyte ageing. This asynchronous cellular ageing may explain the characteristic midlife onset, chronic relapsing course and later life attenuation of melasma. From a therapeutic perspective, effective long-term management of melasma may require not only suppression of persistent melanocyte activation but also modulation of the photoaged dermal microenvironment.
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6. Comment on 'Dermoscopic-Pathologic Correlates of Invasiveness and Nevus Visibility in Nevus-Associated Melanoma'.
PMID:日期:2026-09-01该文献暂无摘要。
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7. Optogenetic Dissection of Sensory Neuron-Macrophage Interactions in Psoriasiform Skin Inflammation: Advances Based on In Vivo Calcium Imaging Techniques.
PMID:日期:2026-09-01Psoriasis represents a chronic inflammatory skin disorder driven by bidirectional neuro-immune crosstalk between cutaneous sensory neurons and tissue macrophages. Tissue-resident macrophages exhibit a continuous functional spectrum rather than rigid binary M1/M2 subsets, and their dynamic reprogramming critically shapes inflammatory onset, perpetuation and resolution; however, conventional experimental approaches cannot readily provide causal, high spatiotemporal-resolution evidence for neuron-macrophage communication in intact skin. Optogenetics combined with intravital in vivo calcium imaging has emerged as a powerful integrated platform to precisely manipulate sensory neuronal activity and simultaneously record real-time calcium signalling dynamics in macrophages. Herein, we review recent advances using this toolkit in psoriasiform skin inflammation. Optogenetic activation of nociceptive sensory neurons triggers rapid macrophage calcium transients primarily mediated by neuropeptide calcitonin gene-related peptide (CGRP). Chronic optogenetic neuronal stimulation is sufficient to initiate psoriasiform lesions, whereas optogenetic silencing can reverse established skin inflammation. Downstream calcium-CaMKII-NF-κB/MAPK cascades drive pro-inflammatory macrophage activation, while sympathetic norepinephrine-dependent β2-adrenergic receptor signalling provides homeostatic negative feedback. A spatiotemporal calcium-wave model further explains focal plaque formation. We also discuss translational bottlenecks for optogenetic techniques and potential therapeutic targets targeting sensory neuron-macrophage axis. Finally, we highlight future multimodal research directions bridging pre-clinical mechanistic findings and clinical translation for psoriasis and other neuro-immune inflammatory skin diseases.
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8. Aquaporin 3 Promoter Polymorphisms Reduce Gene Expression and Associate Altered Autophagy-Related Gene Signatures With Atopic Dermatitis Susceptibility.
PMID:日期:2026-09-01Genome-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 aquaporin 3 (AQP3) 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 AQP3 knockdown on autophagy, skin barrier integrity, and wound closure. A discovery GWAS identified significant association between AD and SNP rs12555686 (p = 1.67 × 10, OR = 1.89), located in the promoter of AQP3. Two additional SNPs in strong LD (rs2231225, rs3758279) formed a major haplotype associated with reduced AQP3 expression. Reduced AQP3 expression was associated with decreased autophagy markers (Beclin1, ATG5, ATG12, GABARAPL2, LAMP2, ATG4C), increased senescence markers (p21, GADD45A, SERPINE1), and elevated inflammatory cytokines (IL8, IL1B, TNF). Lastly, AQP3 knockdown in HaCaT keratinocytes reduced steady-state LC3B-II/LC3B-I ratio, reduced occludin expression, and delayed wound healing in vitro. Promoter variants in AQP3 link genetic susceptibility to gene signatures consistent with altered autophagy, cellular senescence, and inflammation in AD. These findings highlight AQP3 as a potential modulator of both epithelial and immune-related mechanisms in AD pathogenesis.
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10. Elevated SOX9 Expression Is Associated With Extracellular Matrix Remodelling and Aggressive Clinicopathological Features in Extramammary Paget's Disease.
PMID:日期:2026-09-01Extramammary Paget's disease (EMPD) is a rare cutaneous adenocarcinoma that remains clinically challenging in advanced or metastatic stages, yet the molecular mechanisms underlying tumour invasion and metastasis remain poorly understood. SOX9 has emerged as a critical factor in tumour invasion and metastasis across several cancers, but its role in EMPD has not been systematically characterized. In this study, we established a cohort of 93 patients with genital EMPD and performed integrated transcriptomic and proteomic profiling to assess the expression and clinical significance of SOX9. We found that elevated SOX9 transcript levels were significantly associated with tumour invasion, whereas increased SOX9 protein abundance correlated with metastatic progression. To explore the potential functional relevance, we established a SOX9-overexpressing cellular model as a preliminary approach and performed combined transcriptomic and extracellular matrix (ECM) proteomic analyses. Functionally, SOX9 overexpression enhanced cellular migratory capacity in vitro. Both transcriptomic and proteomic profiles converged on the regulation of extracellular matrix organisation, with SOX9 overexpression associated with increased expression of ECM-related genes including MMP1, MMP10 and MMP12, as well as increased abundance of ECM proteins such as FMOD and COL1A2. Collectively, these findings suggest that SOX9 may serve as a promising indicator of aggressive clinicopathological features in EMPD and provide preliminary evidence linking its overexpression to ECM-related molecular changes and enhanced cellular migratory capacity in vitro. Further validation in independent cohorts and functional models is warranted.