Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes.
Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes.
复制标题
自噬功能障碍：破坏黑素细胞氧化还原平衡参与白癜风发病的可能机制
DOI：
10.1155/2016/3401570
复制
发表时间：
2016
影响因子：
--
通讯作者：
Zhang C
中科院分区：
文献类型：
--
作者：
Qiao Z;Wang X;Xiang L;Zhang C
白癜风是一种常见的慢性获得性色素沉着疾病，其特征是表皮和毛囊贮库中功能性黑素细胞的丧失。在白癜风发病机制的多种假说中，自身免疫和氧化应激介导的黑素细胞毒性仍然是最广泛接受的。自噬是一种广泛存在于真核细胞中的溶酶体依赖性降解途径。自噬参与了许多细胞的氧化应激反应，在防止氧化应激引起的损伤中起保护作用。最近的研究已经将自噬登记为限制由UV光和脂质氧化引起的损伤、使表皮角质形成细胞中的氧化应激保持在稳定状态以及维持黑素细胞的正常增殖和老化的重要调节剂。自噬的损伤可能会破坏抗氧化防御系统，使黑素细胞受到氧化损伤。这些发现为探讨白癜风及其他色素沉着疾病的发病机制提供了新的思路。
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.
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DOI：
10.1073/pnas.172398899
发表时间：
2002-09-03
影响因子：
11.1
作者：
Dinkova-Kostova, AT;Holtzclaw, WD;Talalay, P
通讯作者：
Talalay, P
影响因子：
6.5
作者：
Jian, Zhe;Li, Kai;Gao, Tianwen
通讯作者：
Gao, Tianwen
影响因子：
21.3
作者：
Komatsu, Masaaki;Kurokawa, Hirofumi;Yamamoto, Masayuki
通讯作者：
Yamamoto, Masayuki
影响因子：
3.6
作者：
Kim, Eun Sung;Chang, Huikyoung;Cho, Dong-Hyung
通讯作者：
Cho, Dong-Hyung
影响因子：
6.5
作者：
Denat, Laurence;Kadekaro, Ana L.;Marrot, Laurent;Leachman, Sancy A.;Abdel-Malek, Zalfa A.
通讯作者：
Abdel-Malek, Zalfa A.