骨骼肌
恶病质
生物
浪费的
肌肉萎缩
再生(生物学)
合成代谢
肌萎缩
萎缩
运动不耐症
肌生成抑制素
信号转导
肌肉肥大
内分泌学
生物信息学
心力衰竭
内科学
医学
细胞生物学
癌症
遗传学
作者
Marc A. Egerman,David J. Glass
标识
DOI:10.3109/10409238.2013.857291
摘要
The molecular mechanisms underlying skeletal muscle maintenance involve interplay between multiple signaling pathways. Under normal physiological conditions, a network of interconnected signals serves to control and coordinate hypertrophic and atrophic messages, culminating in a delicate balance between muscle protein synthesis and proteolysis. Loss of skeletal muscle mass, termed "atrophy", is a diagnostic feature of cachexia seen in settings of cancer, heart disease, chronic obstructive pulmonary disease, kidney disease, and burns. Cachexia increases the likelihood of death from these already serious diseases. Recent studies have further defined the pathways leading to gain and loss of skeletal muscle as well as the signaling events that induce differentiation and post-injury regeneration, which are also essential for the maintenance of skeletal muscle mass. In this review, we summarize and discuss the relevant recent literature demonstrating these previously undiscovered mediators governing anabolism and catabolism of skeletal muscle.
科研通智能强力驱动
Strongly Powered by AbleSci AI