摘要
废用性肌萎缩主要是由于蛋白质降解增强和蛋白质合成减弱导致的,对调节这一复杂过程的细胞信号通路的研究已取得了重要进展。越来越多的证据表明,活性氧自由基引起的氧化应激是细胞信号通路的重要调节因素,可导致长期废用时蛋白质降解增强和蛋白质合成减弱。本文主要讨论活性氧自由基(reactive oxygen species,ROS)对废用性肌萎缩蛋白质代谢的信号调节作用。
Disuse-induced muscle atrophy results from both the increased proteolysis and decreased protein synthesis. Investigations of cell signal pathways regulating the disuse muscle atrophy have obtained an important progress in the understanding of this complex process. Increasing evidence indicates that the oxidative stress produced by reactive oxygen species （ROS） is a key regulator of cell signal pathways,and leads to increase the proteolysis and muscle atrophy during periods of prolonged disuse. This review will discuss the role of ROS in the pathophysiology of skeletal muscle disuse atrophy.
出处
《国际病理科学与临床杂志》
CAS
2009年第2期156-159,共4页
Journal of International Pathology and Clinical Medicine
关键词
氧自由基
废用性肌萎缩
蛋白质分解
信号传导
reactive oxygen species
disuse-induced muscle atrophy
protein breakdown
signal transduetion
作者简介
孟思进，硕士，副教授，主要从事骨骼肌生理研究。通讯作者：盂思进，E-mail：msijin@wipe．edu．cn
