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线粒体-黑素细胞细胞相互作用:白癜风发病机制的一个新出现的机制。

Mitochondria-Melanocyte cellular interactions: An emerging mechanism of vitiligo pathogenesis.

机构信息

Department of Dermatology, Venereology & Leprology, PGIMER, Chandigarh, 160012, India.

出版信息

J Eur Acad Dermatol Venereol. 2023 Nov;37(11):2196-2207. doi: 10.1111/jdv.19019. Epub 2023 Apr 1.

Abstract

Mitochondria has emerged as a potential modulator of melanocyte function other than just meeting its cellular ATP demands. Mitochondrial DNA defects are now an established cause of maternal inheritance diseases. Recent cellular studies have highlighted the mitochondrial interaction with other cellular organelles that lead to disease conditions such as in Duchenne muscular dystrophy, where defective mitochondria was found in melanocytes of these patients. Vitiligo, a depigmentory ailment of the skin, is another such disorder whose pathogenesis is now found to be associated with mitochondria. The complete absence of melanocytes at the lesioned site in vitiligo is a fact; however, the precise mechanism of this destruction is still undefined. In this review we have tried to discuss and link the emerging facts of mitochondrial function or its inter- and intra-organellar communications in vitiligo pathogenesis. Mitochondrial close association with melanosomes, molecular involvement in melanocyte-keratinocyte communication and melanocyte survival are new paradigm of melanogenesis that could ultimately account for vitiligo. This definitely adds the new dimensions to our understanding of vitiligo, its management and designing of future mitochondrial targeted therapy for vitiligo.

摘要

线粒体除了满足细胞的 ATP 需求外,已成为黑素细胞功能的潜在调节剂。线粒体 DNA 缺陷现在是母系遗传疾病的一个既定原因。最近的细胞研究强调了线粒体与其他细胞细胞器的相互作用,导致了疾病状态,如在杜氏肌营养不良症中,在这些患者的黑素细胞中发现了有缺陷的线粒体。白癜风是皮肤的一种脱色疾病,是另一种与线粒体有关的疾病。在白癜风中,受损部位的黑素细胞完全缺失是事实;然而,这种破坏的确切机制仍未确定。在这篇综述中,我们试图讨论并联系线粒体功能的新出现的事实,或其在白癜风发病机制中的细胞器间和细胞器内的通讯。线粒体与黑素小体的密切关联、分子参与黑素细胞-角质形成细胞通讯和黑素细胞存活是黑素生成的新范例,最终可能导致白癜风。这无疑为我们理解白癜风、其治疗以及为白癜风设计未来的线粒体靶向治疗增加了新的维度。

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