ATM at the crossroads of reactive oxygen species and autophagy.

Abstract

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.

• Authors: Xiaochen Xie, Ye Zhang, Zhuo Wang, Shanshan Wang, Xiaoyou Jiang, Hongyan Cui, Tingting Zhou, Zheng He, Hao Feng, Qiqiang Guo, Xiaoyu Song, Liu Cao
• Journal: International journal of biological sciences (Int J Biol Sci) Vol. 17 Issue 12 Pg. 3080-3090 ( 2021) ISSN: 1449-2288 [Electronic] Australia
• PMID: 34421351 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: © The author(s).

Chemical References

• Reactive Oxygen Species
• ATM protein, human
• Ataxia Telangiectasia Mutated Proteins

Topics

• Animals
• Ataxia Telangiectasia Mutated Proteins (metabolism)
• Autophagy
• Cell Nucleus (metabolism)
• Cytoplasm (metabolism)
• Homeostasis
• Humans
• Reactive Oxygen Species (metabolism)
• Signal Transduction