Reactive oxygen species (ROS) are generally small, short-lived and highly reactive molecules, initially thought to be a pathological role in the cell. A growing amount of evidence in recent years argues for ROS functioning as a signaling intermediate to facilitate cellular adaptation in response to pathophysiological stress through the regulation of autophagy. Autophagy is an essential cellular process that plays a crucial role in recycling cellular components and damaged organelles to eliminate sources of ROS in response to various stress conditions. A large number of studies have shown that DNA damage response (DDR) transducer ataxia-telangiectasia mutated (ATM) protein can also be activated by ROS, and its downstream signaling pathway is involved in autophagy regulation. This review aims at providing novel insight into the regulatory mechanism of ATM activated by ROS and its molecular basis for inducing autophagy, and revealing a new function that ATM can not only maintain genome homeostasis in the nucleus, but also as a ROS sensor trigger autophagy to maintain cellular homeostasis in the cytoplasm.

中文翻译：

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ATM 处于活性氧和自噬的十字路口


活性氧（ROS）通常是小、寿命短且高反应性的分子，最初被认为在细胞中具有病理作用。近年来，越来越多的证据表明，ROS 作为信号传导中间体，通过调节自噬促进细胞适应病理生理应激。自噬是一个重要的细胞过程，在回收细胞成分和受损细胞器、消除ROS来源以应对各种应激条件方面发挥着至关重要的作用。大量研究表明DNA损伤反应（DDR）转导共济失调毛细血管扩张突变（ATM）蛋白也能被ROS激活，其下游信号通路参与自噬调节。本综述旨在对ROS激活ATM的调控机制及其诱导自噬的分子基础提供新的见解，揭示ATM不仅可以维持细胞核内基因组稳态，而且可以作为ROS传感器触发自噬的新功能。维持细胞质内的细胞稳态。