|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|1907658||1534945||2016||10 صفحه PDF||سفارش دهید||دانلود رایگان|
• Autophagy regulates skeletal muscle homeostasis.
• Skeletal muscle atrophy occurs due to increased autophagy.
• Impaired autophagy leads skeletal muscle degeneration due to accumulation of damaged proteins and organelles.
• Regulation of skeletal muscle autophagy by reactive oxygen species is due to sub-cellular production of ROS.
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.
Journal: Free Radical Biology and Medicine - Volume 98, September 2016, Pages 103–112