Journal of dermatological science最新文献

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IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/S0923-1811(25)00089-1

引用次数: 0

Councilor’s Meeting/General Assembly of Members at the 49th Annual General Meeting of the Japanese Society for Investigative Dermatology (JSID) 日本皮肤病调查学会（JSID）第49届年会委员会议/会员大会

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.013

引用次数: 0

Overexpression of FOXM1 drives mycosis fungoides progression by regulating the cell cycle FOXM1的过表达通过调节细胞周期驱动蕈样真菌病的进展。

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.010

Kecen Liu , Huizhong Wang , Jingyang Dang , Jiajia Zhu , Yujie Wen , Zhuojing Chen , Yang Wang , Jingru Sun

Background

Mycosis fungoides (MF), the most prevalent variant of cutaneous T-cell lymphoma (CTCL), is characterized by the clonal proliferation of skin-homing CD4+ T lymphocytes. Forkhead box M1 (FOXM1) plays significant roles in the progression of various solid tumors. Its expression has been reported to diminish following treatment with Neosetophomone B in CTCL cells in vitro. However, the role of FOXM1 in the pathogenesis of MF remains unclear.

Objectives

To evaluate the expression pattern and underlying mechanism of FOXM1 in MF.

Methods

FOXM1 expression in lesional skin samples was accessed via immunohistochemistry analyses. Inhibition of FOXM1 was performed through lenti-virus shRNA vector mediated gene knockdown and treatment with specific FOXM1 inhibitors (RCM1 and FDI-6). Furthermore, animal experiments were conducted to evaluate the effects of FOXM1 knockdown or treatment with FOXM1 inhibitors on tumor growth in vivo.

Results

Overexpression of FOXM1 was observed in MF with a stage-dependent pattern and poor prognosis. Inhibition of FOXM1 via either shRNA or specific inhibitors, significantly impaired MF cell proliferation by inducing cell cycle arrest and apoptosis, while also suppressing tumorigenicity in vitro and in vivo. Transcriptomic analysis revealed that FOXM1 suppression led to the downregulation of genes involved in cell cycle regulation, including CCNB2, CDK1, and E2F1.

Conclusions

The overexpression of FOXM1 contributes significantly to the progression of MF primarily by regulating the cell cycle. Furthermore, FOXM1 may serve as a reliable prognostic biomarker and a promising therapeutic target for MF.

背景：蕈样真菌病（Mycosis fungoides， MF）是皮肤T细胞淋巴瘤（CTCL）最常见的变种，其特征是皮肤归巢CD4+ T淋巴细胞的克隆性增殖。叉头盒M1 （Forkhead box M1, FOXM1）在多种实体肿瘤的进展中起重要作用。据报道，在体外CTCL细胞中，Neosetophomone B治疗后其表达减少。然而，FOXM1在MF发病机制中的作用尚不清楚。目的：探讨FOXM1在MF中的表达规律及其机制。方法：采用免疫组化方法检测病变皮肤标本中FOXM1的表达。FOXM1的抑制是通过慢病毒shRNA载体介导的基因敲低和特异性FOXM1抑制剂（RCM1和FDI-6）进行的。此外，我们还进行了动物实验来评估FOXM1敲除或FOXM1抑制剂治疗对体内肿瘤生长的影响。结果：MF中FOXM1过表达，呈分期依赖性，预后较差。通过shRNA或特异性抑制剂抑制FOXM1，通过诱导细胞周期阻滞和凋亡显著损害MF细胞增殖，同时在体外和体内抑制致瘤性。转录组学分析显示FOXM1抑制导致参与细胞周期调控的基因下调，包括CCNB2、CDK1和E2F1。结论：FOXM1过表达主要通过调控细胞周期参与MF的进展。此外，FOXM1可能作为可靠的预后生物标志物和有希望的MF治疗靶点。

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引用次数: 0

Oculocutaneous albinism type 1B associated with allelic combination of a risk haplotype 1B型皮肤白化病与风险单倍型等位基因组合相关。

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.007

Nikoletta Nagy , Aliasgari Abdolreza , Margit Pál , Barbara Anna Bokor , Amarilla Barcsay-Veres , Noémi Ágnes Varga , Márta Medvecz , Viktória Szabó , Márta Széll

引用次数: 0

SERPINA12 variants harboured in Nagashima-type palmoplantar keratoderma: Potential inflammatory characteristics 长岛型掌足底角化病中携带的SERPINA12变异：潜在的炎症特征

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.009

Cheng Zhang , Yumeng Wang , Qiaoyu Cao , Hongsong Ge , Xinjie Lin , Xinyi Wang , Anqi Zhao , Wei He , Qin Zeng , Haisheng Huang , Qin Yan , Ming Li

引用次数: 0

Landscapes of gut microbiome and metabolic signatures in vitiligo patients with co-morbid emotional distress 伴有共病情绪困扰的白癜风患者肠道微生物群和代谢特征的景观。

IF 4.6

Journal of dermatological science

Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.011

Mei Luan , Binyue Mao , Yixin Zhao , Jianan Chen , Pengju Yang , Weizhe Li , Hao Lei , Yi Yang , Wenwan Chang , Kuanhou Mou , Pan Li

Background

Vitiligo is a depigmentation disorder frequently associated with emotional distress; however, the precise mechanisms underlying this co-morbidity remain unclear.

Objective

This study aims to investigate whether gut dysbiosis and gut metabolites contributes to emotional distress in patients with vitiligo.

Methods

Depression and anxiety were assessed using the Patient Health Questionnaire-9 and Generalized Anxiety Disorder-7, respectively. Totally enrolled 28 vitiligo patients were diagnosed with depression or anxiety (VWD), 44 without such conditions (VTD), and 37 healthy controls (HC). Stool samples were analyzed using 16S rRNA gene sequencing and liquid chromatography triple quadrupole tandem mass spectrometry.

Results

The intestinal flora of VWD group changed significantly with reduced α-diversity. The β-diversity varied among groups. Megasphaera and Anaerostipes increased in the VWD group, whereas Bilophila etc. decreased. Linear Discriminant Analysis Effect Size revealed Lachnoclostridium as a representative flora in the VWD and Faecalibacterium as a representative flora in the VTD. Metabolites such as L-glutamic acid and indole were lower in the VWD group than in the HC, while oleamide, cuminaldehyde, and taurine were higher in the VWD with VTD group. Lachnoclostridium negatively correlated with indole and L-glutamic acid. This study identified notable variations in pathways involved in the biosynthesis of phenylalanine, tyrosine, and tryptophan bile secretion, GABAergic synapses, and taurine and hypotaurine metabolism between the VWD and HC groups.

Conclusion

Specific fecal microbes and metabolites may contribute to the pathogenesis of VWD. These findings provide a novel perspective for addressing emotional distress in patients with vitiligo by targeting the gut-brain-skin axis.

背景：白癜风是一种色素脱失性疾病，通常与情绪困扰有关；然而，这种合并症的确切机制尚不清楚。目的：本研究旨在探讨肠道生态失调和肠道代谢物是否与白癜风患者的情绪困扰有关。方法：分别使用患者健康问卷-9和广泛性焦虑障碍-7对抑郁和焦虑进行评估。共有28例白癜风患者被诊断为抑郁或焦虑（VWD）， 44例无抑郁或焦虑（VTD）， 37例健康对照（HC）。粪便样品采用16S rRNA基因测序和液相色谱三重四极杆串联质谱分析。结果：VWD组肠道菌群变化明显，α-多样性降低。β-多样性在不同群体间存在差异。VWD组巨噬菌和厌氧菌数量增加，嗜菌等数量减少。线性判别分析效应大小显示Lachnoclostridium是VWD的代表菌群，Faecalibacterium是VTD的代表菌群。VWD组的代谢产物如l -谷氨酸和吲哚低于HC组，而VWD合并VTD组的油酰胺、茴香醛和牛磺酸高于HC组。Lachnoclostridium与吲哚和l -谷氨酸呈负相关。本研究发现，在VWD组和HC组之间，涉及苯丙氨酸、酪氨酸和色氨酸的生物合成、gaba能突触以及牛磺酸和次牛磺酸代谢的途径存在显著差异。结论：特定的粪便微生物和代谢物可能参与了VWD的发病机制。这些发现为针对肠道-脑-皮肤轴治疗白癜风患者的情绪困扰提供了一个新的视角。

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引用次数: 0

The role of PPARs family members in acne ppar家族成员在痤疮中的作用。

IF 4.6

Journal of dermatological science

Pub Date : 2025-05-23 DOI: 10.1016/j.jdermsci.2025.04.003

Shaoyang Zhang , Yating Yang , Li Yang, Fangyu Meng, Yizhe Mu, Yuhang Yuan, Yuan Zhang

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that play a crucial role in the genetic regulation of lipid metabolism and energy homeostasis. There is increasing evidence to suggest that PPARs may have a significant impact on the development and progression of acne, including its role in regulating lipid production, inhibiting keratinocyte proliferation, and reducing acne-related inflammation. As such, PPARs present themselves as promising therapeutic targets for both the prevention and treatment of acne. This article provides an overview of the role of PPARs in the pathological processes underlying acne, with particular emphasis on inflammation and lipid regulation.

过氧化物酶体增殖体激活受体（PPARs）是配体激活的转录因子，在脂质代谢和能量稳态的遗传调控中起着至关重要的作用。越来越多的证据表明，ppar可能对痤疮的发生和发展有重要影响，包括其调节脂质产生、抑制角化细胞增殖和减少痤疮相关炎症的作用。因此，ppar作为预防和治疗痤疮的有希望的治疗靶点。本文概述了ppar在痤疮病理过程中的作用，特别强调炎症和脂质调节。

引用次数: 0

PRRX1 is a key regulator in the phenotypic transition between human normal dermal and keloid fibroblasts PRRX1是人类正常真皮和瘢痕疙瘩成纤维细胞表型转换的关键调节因子。

IF 4.6

Journal of dermatological science

Pub Date : 2025-05-16 DOI: 10.1016/j.jdermsci.2025.05.002

Shuqian Dou , Fengyu Zhang , Yongjing He , Pan Du , Yue Deng , Mingkun Shao , Guoxun Yang , Kongjia Wu , Yueqin Zeng , Cheng Peng , Wenjun Liu

Background

Scarring after skin trauma is a major clinical challenge, as it affects patients’ appearance and function.

Objective

Given that human foetal skin possesses scarless wound healing ability, we aimed to understand the differences among human foetal skin, postnatal skin, and keloid tissue to find out the key factors affecting wound healing outcome.

Methods

We used spatial transcriptomics (ST), histological imaging, and other methods to investigate the cellular and molecular characteristics underlying scarless healing by comparing these skin types.

Results

We identified histological and cellular differences among these samples, including the extracellular matrix, hair follicles, stem cells, and immune cells. Significant heterogeneity was found in fibroblasts across all samples. Among these fibroblast subpopulations, the proportion of paired related homeobox 1 (PRRX1)-positive fibroblast increased from foetus to postnatal skin (PS) and further in keloids. We validated PRRX1’s roles in regulating the phenotypic transition between normal and keloid fibroblasts. A three-dimensional human keloid model was used to further confirm its roles at the tissue level.

Conclusions

In summary, our work explores the unique characteristics of foetal skin and identifies an important transcription factor in regulating scarless healing, which provides the translational potential for future clinical treatments aimed at promoting scarless wound healing.

背景：皮肤创伤后瘢痕形成是一个重大的临床挑战，因为它影响患者的外观和功能。目的：鉴于人类胎儿皮肤具有无疤痕的创面愈合能力，我们旨在了解人类胎儿皮肤与出生后皮肤和瘢痕疙瘩组织的差异，找出影响创面愈合结果的关键因素。方法：通过比较这些皮肤类型，我们使用空间转录组学（ST）、组织学成像和其他方法来研究无疤痕愈合背后的细胞和分子特征。结果：我们确定了这些样本之间的组织学和细胞差异，包括细胞外基质、毛囊、干细胞和免疫细胞。在所有样本的成纤维细胞中发现了显著的异质性。在这些成纤维细胞亚群中，配对相关同源盒1 （PRRX1）阳性成纤维细胞的比例从胎儿到出生后皮肤（PS）增加，在瘢痕疙瘩中进一步增加。我们验证了PRRX1在调节正常瘢痕疙瘩成纤维细胞和瘢痕疙瘩成纤维细胞之间的表型转变中的作用。使用三维人体瘢痕疙瘩模型进一步确认其在组织水平上的作用。结论：总之，我们的工作探索了胎儿皮肤的独特特征，并确定了调节无疤痕愈合的重要转录因子，这为未来旨在促进无疤痕伤口愈合的临床治疗提供了转化潜力。

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引用次数: 0

Stratum corneum pH and ceramides: Key regulators and biomarkers of skin barrier function in atopic dermatitis 角质层pH值和神经酰胺：特应性皮炎中皮肤屏障功能的关键调节因子和生物标志物

IF 4.6

Journal of dermatological science

Pub Date : 2025-05-01 DOI: 10.1016/j.jdermsci.2025.04.001

Takashi Sakai , Yutaka Hatano

The skin, as the outermost layer of the body, serves as a crucial protective barrier against environmental insults while maintaining homeostasis. Atopic dermatitis (AD), a chronic inflammatory skin disorder characterized by recurrent eczema and type 2 inflammation, affects a significant global population. The pathophysiology of AD is closely linked to skin barrier dysfunction, which contributes to increased permeability, immune dysregulation, and microbial imbalances. Historically, skin barrier research has centered on the stratum corneum (SC) and intercellular lipids within the epidermis, primarily conceptualized through the "brick-and-mortar" model. However, recent advancements have revealed a more intricate interplay among various barrier components. Two key determinants of skin barrier—SC pH and SC ceramides—have gained substantial attention. Elevated SC pH leads to enhanced serine protease activity, impaired lipid metabolism, and microbiome dysbiosis, all of which exacerbate barrier dysfunction and inflammation in AD. Concurrently, alterations in SC ceramide profiles and structures compromise skin barrier function. Emerging evidence underscores the potential of SC pH and ceramides as biomarkers for disease progression and as therapeutic targets for barrier restoration. Advances in lipid analyses and non-invasive pH assessment offer promising prospects for personalized dermatologic interventions. This review explores the complex interactions of SC pH and ceramides in AD pathogenesis, discussing their implications for predicting disease flares, guiding treatment strategies, and identifying novel drug targets. A deeper understanding of these mechanisms could pave the way for next-generation therapeutic approaches in AD and other skin barrier-related disorders.

皮肤，作为身体的最外层，在维持体内平衡的同时，也是抵御环境侵害的重要保护屏障。特应性皮炎（AD）是一种以复发性湿疹和2型炎症为特征的慢性炎症性皮肤病，影响着全球大量人群。AD的病理生理学与皮肤屏障功能障碍密切相关，皮肤屏障功能障碍导致渗透性增加、免疫失调和微生物失衡。从历史上看，皮肤屏障研究主要集中在角质层（SC）和表皮内的细胞间脂质上，主要通过“砖瓦”模型概念化。然而，最近的进展揭示了各种屏障成分之间更复杂的相互作用。皮肤屏障的两个关键决定因素- SC pH和SC神经酰胺-已经获得了大量的关注。SC pH升高导致丝氨酸蛋白酶活性增强，脂质代谢受损，微生物群失调，所有这些都加剧了AD的屏障功能障碍和炎症。同时，SC神经酰胺剖面和结构的改变会损害皮肤屏障功能。新出现的证据强调SC pH和神经酰胺作为疾病进展的生物标志物和屏障恢复的治疗靶点的潜力。脂质分析和非侵入性pH值评估的进展为个性化皮肤病学干预提供了广阔的前景。这篇综述探讨了SC pH和神经酰胺在AD发病机制中的复杂相互作用，讨论了它们在预测疾病爆发、指导治疗策略和确定新的药物靶点方面的意义。对这些机制的深入了解可以为阿尔茨海默病和其他皮肤屏障相关疾病的下一代治疗方法铺平道路。

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引用次数: 0

Immune signatures across different stages of cutaneous squamous cell carcinoma 皮肤鳞状细胞癌不同阶段的免疫特征。

IF 4.6

Journal of dermatological science

Pub Date : 2025-05-01 DOI: 10.1016/j.jdermsci.2025.03.002

Laure Favot-Laforge , Elodie Muzotte , Walid Mahfouf , Jerome Rambert , Muriel Cario , François Moisan , Lea Dousset , Hamid-Reza Rezvani

引用次数: 0

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