Redox regulation of autophagy in skeletal muscle.
Redox regulation of autophagy in skeletal muscle.
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DOI：
10.1016/j.freeradbiomed.2016.05.010
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发表时间：
2016-09
影响因子：
7.4
通讯作者：
Abo-Zahrah R
中科院分区：
文献类型：
--
作者：
Rodney GG;Pal R;Abo-Zahrah R
自噬是一种细胞降解途径，其涉及将细胞质组分（包括蛋白质和细胞器）递送至溶酶体进行降解。自噬与骨骼肌的维持有关;自噬增加导致肌肉萎缩，而自噬减少导致退化和虚弱。越来越多的研究表明，活性氧（ROS）是控制自噬的重要细胞信号转导。烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶和线粒体是骨骼肌中ROS产生的主要来源，其可能基于ROS信号的定位通过不同的信号级联调节自噬。本文就骨骼肌自噬的氧化还原调控机制进行综述。了解ROS调控自噬的机制将为骨骼肌疾病提供新的治疗靶点。
Autophagy is a cellular degradative pathway that involves the delivery of cytoplasmic components, including proteins and organelles, to the lysosome for degradation. Autophagy is implicated in the maintenance of skeletal muscle; increased autophagy leads to muscle atrophy while decreased autophagy leads to degeneration and weakness. A growing body of work suggests that reactive oxygen species (ROS) are important cellular signal transducers controlling autophagy. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and mitochondria are major sources of ROS generation in skeletal muscle that are likely regulating autophagy through different signaling cascades based on localization of the ROS signals. This review aims to provide insight into the redox control of autophagy in skeletal muscle. Understanding the mechanisms by which ROS regulate autophagy will provide novel therapeutic targets for skeletal muscle diseases.