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Editors choice 编辑的选择
IF 4.6 Pub Date : 2025-08-01 DOI: 10.1016/S0923-1811(25)00135-5
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引用次数: 0
Healthy skin, Healthy brain 健康的皮肤,健康的大脑。
IF 4.6 Pub Date : 2025-08-01 DOI: 10.1016/j.jdermsci.2025.06.001
Kyeong-No Yoon , Jin Ho Chung
Skin aging extends beyond aesthetic concerns and is increasingly recognized as a key contributor to brain aging through neuroendocrine, inflammatory, and neurochemical mechanisms. Traditionally considered as a peripheral barrier, the skin is now recognized as a neuroendocrine organ capable of communicating with the central nervous system (CNS) via hormone secretion, cytokine signaling, and neurotransmitter modulation. Recent literature has begun to formalize the concept of the skin–brain axis as a bidirectional communication system, particularly within the contexts of psychodermatology and neuroimmunology. This review highlights how extrinsic factors such as ultraviolet (UV) radiation and intrinsic aging disrupt skin homeostasis and trigger systemic effects on brain functions. Chronic UV exposure activates the cutaneous hypothalamic-pituitary-adrenal (HPA) axis and increases systemic cortisol levels, impairing hippocampal neurogenesis and cognitive function. UV-induced alterations in neurotransmitters including glutamate, dopamine, and β-endorphins affect learning, memory, and emotion regulation. Importantly, both photoaging and natural skin aging are associated with reduced synthesis of brain-derived neurotrophic factor (BDNF) in the skin, potentially diminishing systemic BDNF availability, and contributing to cognitive decline. Recent studies explored the protective effects of sunscreen and moisturizers in mitigating cutaneous inflammation and reducing neurodegenerative risk. Additionally, topical or dietary interventions, such as plant-derived polyphenols, may restore skin BDNF levels and enhance skin-brain resilience. Collectively, these findings support a paradigm shift: preserving skin health is not only a dermatological goal, but also a promising strategy for mitigating brain aging and promoting cognitive resilience.
皮肤老化已经超越了审美问题,并且越来越多地被认为是通过神经内分泌、炎症和神经化学机制导致大脑衰老的关键因素。传统上,皮肤被认为是外周屏障,现在被认为是一个神经内分泌器官,能够通过激素分泌、细胞因子信号传导和神经递质调节与中枢神经系统(CNS)进行交流。最近的文献已经开始将皮肤-脑轴的概念形式化为一个双向交流系统,特别是在心理皮肤病学和神经免疫学的背景下。这篇综述强调了外在因素如紫外线(UV)辐射和内在衰老如何破坏皮肤稳态并引发对大脑功能的系统性影响。慢性紫外线照射激活皮肤下丘脑-垂体-肾上腺(HPA)轴,增加全身皮质醇水平,损害海马神经发生和认知功能。紫外线诱导的神经递质改变,包括谷氨酸、多巴胺和β-内啡肽,影响学习、记忆和情绪调节。重要的是,光老化和自然皮肤老化都与皮肤中脑源性神经营养因子(BDNF)合成减少有关,可能会降低全身BDNF的可用性,并导致认知能力下降。最近的研究探索了防晒霜和保湿剂在减轻皮肤炎症和降低神经退行性疾病风险方面的保护作用。此外,局部或饮食干预,如植物源性多酚,可能恢复皮肤BDNF水平,增强皮肤-脑弹性。总的来说,这些发现支持了一种范式转变:保持皮肤健康不仅是皮肤学的目标,也是缓解大脑衰老和促进认知弹性的一种有希望的策略。
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引用次数: 0
C-C motif chemokine receptor 7 (CCR7) in the spinal cord inhibits chronic itch through the neuropeptide NPY 脊髓C-C基序趋化因子受体7 (CCR7)通过神经肽NPY抑制慢性瘙痒。
IF 4.6 Pub Date : 2025-08-01 DOI: 10.1016/j.jdermsci.2025.05.001
Yanying Tan , Zhongqiu Zhao , Xue Luo , Xuebin Han , Hui Xiong , Zhinan Mei

Background

Studies showed that C-C motif chemokine receptor 7 (CCR7) contributes to the maintenance of neuropathic pain. However, whether CCR7 is involved in chronic itch remains unclear.

Objective

To explore the relationship between CCR7 and chronic itch.

Methods

The scratching behavior of wild-type (WT) and Ccr7-/- mice in acute and chronic itch models, or of WT mice in chronic itch after intrathecal injection of CCR7 neutralizing antibody was compared. Mechanical, thermal, and inflammatory pain responses of Ccr7-/- mice and WT mice were examined. The expression of CCR7, some known lamina-specific markers, and itch-related mediators in the spinal cord of WT and Ccr7-/- mice with chronic itch were detected by immunostaining and qRT-PCR respectively. Finally, to explore the possible relationship between CCR7 and Neuropeptide Y (NPY), intrathecal injection of CCR7-siRNA for in vivo knockdown and neurotoxin bombesin-saporin for GRPR-expressing cells ablation were used.

Results

Ccr7-/- mice displayed increasing scratching in chronic itch models. CCR7 neutralizing antibody elevated, while CCR7 ligands CCL19/CCL21 alleviated the scratching behavior in chronic itch models. However, the responses of Ccr7-/- mice to mechanical, thermal, and inflammatory pain did not differ from their WT controls. Also, CCR7+ interneurons co-express NPY, and CCR7 expression was enhanced in the spinal cord of mice with chronic itch. Furthermore, spinal NPY expression was down-regulated in Ccr7-/- mice or after CCR7-siRNA. Finally, GRPR+ neuron ablation eliminated scratching behavior in chronic itch mice regardless of whether the mice lacked CCR7.

Conclusion

Spinal CCR7 mediates persistent itch through a neural network with the inhibitory neuropeptide NPY.
背景:研究表明C-C基序趋化因子受体7 (CCR7)参与神经性疼痛的维持。然而,CCR7是否参与慢性瘙痒尚不清楚。目的:探讨CCR7与慢性瘙痒的关系。方法:比较野生型(WT)和Ccr7-/-小鼠急性和慢性瘙痒模型以及慢性瘙痒小鼠鞘内注射Ccr7中和抗体后的抓痕行为。研究了Ccr7-/-小鼠和WT小鼠的机械、热和炎症性疼痛反应。采用免疫染色法和qRT-PCR分别检测慢性瘙痒小鼠和慢性瘙痒小鼠脊髓中CCR7、部分已知板特异性标记物和瘙痒相关介质的表达。最后,为了探索CCR7与神经肽Y (NPY)之间的可能关系,我们使用鞘内注射CCR7- sirna进行体内敲除,并使用神经毒素炸弹素皂苷进行grpr表达细胞消融。结果:Ccr7-/-小鼠在慢性瘙痒模型中表现出增加的抓痕。CCR7中和抗体升高,CCR7配体CCL19/CCL21减轻慢性瘙痒模型的抓痕行为。然而,Ccr7-/-小鼠对机械性、热性和炎症性疼痛的反应与WT对照组没有差异。CCR7+中间神经元共表达NPY, CCR7在慢性瘙痒小鼠脊髓中的表达增强。此外,Ccr7-/-小鼠或Ccr7- sirna后脊髓NPY表达下调。最后,无论小鼠是否缺乏CCR7, GRPR+神经元消融均可消除慢性瘙痒小鼠的抓痕行为。结论:脊髓CCR7通过抑制神经肽NPY的神经网络介导持续瘙痒。
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引用次数: 0
Editors Choice 编辑的选择
IF 4.6 Pub Date : 2025-06-24 DOI: 10.1016/S0923-1811(25)00106-9
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引用次数: 0
Editors Choice 编辑的选择
IF 4.6 Pub Date : 2025-06-01 DOI: 10.1016/S0923-1811(25)00089-1
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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 Pub Date : 2025-06-01 DOI: 10.1016/j.jdermsci.2025.04.013
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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 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 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
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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 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
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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 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
期刊
Journal of dermatological science
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