Department of Neurobiology, Physiology and Behavior, University of California, Davis, One Shields Avenue, Davis, CA 95616, United States.
Int J Biochem Cell Biol. 2013 Oct;45(10):2200-8. doi: 10.1016/j.biocel.2013.06.011. Epub 2013 Jun 22.
Loss of skeletal muscle mass occurs frequently in clinical settings in response to joint immobilization and bed rest, and is induced by a combination of unloading and inactivity. Disuse-induced atrophy will likely affect every person in his or her lifetime, and can be debilitating especially in the elderly. Currently there are no good therapies to treat disuse-induced muscle atrophy, in part, due to a lack of understanding of the cellular and molecular mechanisms responsible for the induction and maintenance of muscle atrophy. Our current understanding of disuse atrophy comes from the investigation of a variety of models (joint immobilization, hindlimb unloading, bed rest, spinal cord injury) in both animals and humans. Under conditions of unloading, it is widely accepted that there is a decrease in protein synthesis, however, the role of protein degradation, especially in humans, is debated. This review will examine the current understanding of the molecular and cellular mechanisms regulating muscle loss under disuse conditions, discussing the similarities and areas of dispute between the animal and human literature. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
肌肉骨骼质量的丧失在临床环境中经常发生,是关节固定和卧床休息的反应,是由卸载和不活动的组合引起的。废用性萎缩可能会影响每个人的一生,尤其是在老年人中,这种萎缩可能会导致身体虚弱。目前,还没有很好的治疗方法来治疗废用性肌肉萎缩,部分原因是对导致肌肉萎缩的诱导和维持的细胞和分子机制缺乏了解。我们目前对废用性萎缩的认识来自于对动物和人类各种模型(关节固定、下肢卸载、卧床休息、脊髓损伤)的研究。在卸载条件下,人们普遍认为蛋白质合成减少,然而,蛋白质降解的作用,特别是在人类中,是有争议的。这篇综述将探讨在废用条件下调节肌肉丧失的分子和细胞机制的最新认识,讨论动物和人类文献之间的相似之处和争议领域。本文是主题为“肌肉消耗的分子基础”的定向问题的一部分。