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自噬功能障碍:一种可能通过打破黑素细胞氧化还原平衡参与白癜风发病机制的机制。

Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes.

作者信息

Qiao Zhuhui, Wang Xiuxiu, Xiang Leihong, Zhang Chengfeng

机构信息

Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

Oxid Med Cell Longev. 2016;2016:3401570. doi: 10.1155/2016/3401570. Epub 2016 Nov 29.

Abstract

Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of functional melanocytes from the epidermis and follicular reservoir. Among multiple hypotheses which have been proposed in the pathogenesis of vitiligo, autoimmunity and oxidative stress-mediated toxicity in melanocytes remain most widely accepted. Macroautophagy is a lysosome-dependent degradation pathway which widely exists in eukaryotic cells. Autophagy participates in the oxidative stress response in many cells, which plays a protective role in preventing damage caused by oxidative stress. Recent studies have enrolled autophagy as an important regulator in limiting damage caused by UV light and lipid oxidation, keeping oxidative stress in a steady state in epidermal keratinocytes and maintaining normal proliferation and aging of melanocytes. Impairment of autophagy might disrupt the antioxidant defense system which renders melanocytes to oxidative insults. These findings provide supportive evidence to explore new ideas of the pathogenesis of vitiligo and other pigmentation disorders.

摘要

白癜风是一种常见的慢性获得性色素沉着障碍,其特征是表皮和毛囊储备中功能性黑素细胞丧失。在白癜风发病机制中提出的多种假说中,自身免疫和黑素细胞中氧化应激介导的毒性仍然是最被广泛接受的。巨自噬是一种依赖溶酶体的降解途径,广泛存在于真核细胞中。自噬参与许多细胞的氧化应激反应,在预防氧化应激引起的损伤方面发挥保护作用。最近的研究已将自噬作为限制紫外线和脂质氧化造成损伤、使表皮角质形成细胞中的氧化应激保持稳定状态以及维持黑素细胞正常增殖和衰老的重要调节因子。自噬受损可能会破坏抗氧化防御系统,使黑素细胞易受氧化损伤。这些发现为探索白癜风和其他色素沉着障碍发病机制的新思路提供了支持性证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a810/5153471/1c54344ded02/OMCL2016-3401570.001.jpg

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