Autophagy is a process involving the self-digestion of components that participates in anti-oxidative stress responses and protects cells against oxidative damage. However, the role of autophagy in the anti-oxidative stress responses of melanocytes remains unclear. To investigate the role of autophagy in human epidermal melanocytes, we knocked down and overexpressed ATG7, the critical gene of autophagy, in normal human epidermal melanocytes. We demonstrated that ATG7-dependent autophagy could affect melanin content of melanocytes by regulating melanogenesis. Moreover, suppression of ATG7-dependent autophagy inhibits proliferation and promotes oxidative stress-induced apoptosis of melanocytes, whereas enhancement of ATG7-dependent autophagy protects melanocytes from oxidative stress-induced apoptosis. Meanwhile, deficiency of ATG7-dependent autophagy results in premature senescence of melanocytes under oxidative stress. Notably, we verified that ATG7-dependent autophagy could alter oxidative stress homeostasis by regulating reactive oxygen species (ROS) production, nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, and the activity of several antioxidant enzymes in melanocytes. In conclusion, our study suggested that ATG7-dependent autophagy is indispensable for redox homeostasis and the biological functions of melanocytes, such as melanogenesis, proliferation, apoptosis, and senescence, especially under oxidative stress.

中文翻译：

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ATG7 依赖性自噬功能障碍会导致抗氧化反应失调，并导致氧化应激诱导的人表皮黑素细胞生物损伤。

自噬是一个涉及参与抗氧化应激反应并保护细胞免受氧化损伤的成分的自我消化的过程。然而，自噬在黑素细胞抗氧化应激反应中的作用仍不清楚。为了研究自噬在人表皮黑素细胞中的作用，我们在正常人表皮黑素细胞中敲低并过度表达自噬的关键基因 ATG7。我们证明ATG7依赖性自噬可以通过调节黑色素生成来影响黑色素细胞的黑色素含量。此外，抑制 ATG7 依赖性自噬可抑制增殖并促进氧化应激诱导的黑素细胞凋亡，而增强 ATG7 依赖性自噬可保护黑素细胞免受氧化应激诱导的细胞凋亡。同时，ATG7依赖性自噬的缺陷导致氧化应激下黑素细胞过早衰老。值得注意的是，我们验证了 ATG7 依赖性自噬可以通过调节活性氧 (ROS) 的产生、核因子红细胞 2 相关因子 2 (Nrf2) 抗氧化途径以及黑素细胞中几种抗氧化酶的活性来改变氧化应激稳态。总之，我们的研究表明，ATG7 依赖性自噬对于氧化还原稳态和黑素细胞的生物学功能（例如黑素生成、增殖、凋亡和衰老）是不可或缺的，尤其是在氧化应激下。