Autophagy as a regulator of cardiovascular redox homeostasis.
Autophagy as a regulator of cardiovascular redox homeostasis.
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DOI：
10.1016/j.freeradbiomed.2016.12.003
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发表时间：
2017-08
影响因子：
7.4
通讯作者：
Finkel T
中科院分区：
文献类型：
--
作者：
Yan Y;Finkel T
自噬是一个高度调控的过程，涉及通过溶酶体介导的途径从细胞和组织中去除受损的蛋白质和细胞器。越来越多的证据表明，自噬是维持氧化还原稳态所必需的。在这里，我们探讨自噬和活性氧（ROS）之间的联系。特别是，我们讨论了氧化依赖的信号如何调节自噬通量，以及自噬如何反过来调节ROS水平。最后，我们讨论了自噬的下降或破坏如何导致氧化还原依赖性心血管病理，并帮助促进心血管功能的年龄依赖性下降。
Autophagy is a highly regulated process involving the removal of damaged proteins and organelles from cells and tissues through a lysosomal-mediated pathway. Accumulating evidence suggests that autophagy is necessary to maintain redox homeostasis. Here, we explore the connection between autophagy and reactive oxygen species (ROS). In particular, we discuss how oxidant-dependent signaling can modulate autophagic flux and how autophagy can, in turn, modulate ROS levels. Finally, we discuss how a decline or disruption of autophagy might contribute to redox-dependent cardiovascular pathology and help fuel the age-dependent decline in cardiovascular function.