Emerging molecular mediators and targets for age-related skeletal muscle atrophy

被引:14
作者
Brown, Lemuel A. [1 ,2 ]
Guzman, Steve D. [1 ,2 ]
Brooks, Susan, V [1 ,2 ]
机构
[1] Univ Michigan, Dept Mol & Integrat Physiol, 2029 BSRB,109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Dept Biomed Engn, Ann Arbor, MI 48109 USA
关键词
CUZN-SUPEROXIDE-DISMUTASE; NEUROMUSCULAR-JUNCTION; OXIDATIVE STRESS; BODY-COMPOSITION; GROWTH-HORMONE; REPLACEMENT THERAPY; PROLONGED EXERCISE; UBIQUITIN LIGASES; SARCOPENIA FACTS; O-GLYCOSYLATION;
D O I
10.1016/j.trsl.2020.03.001
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
The age-associated decline in muscle mass has become synonymous with physical frailty among the elderly due to its major contribution in reduced muscle function. Alterations in protein and redox homeostasis along with chronic inflammation, denervation, and hormonal dysregulation are all hallmarks of muscle wasting and lead to clinical sarcopenia in older adults. Reduction in skeletal muscle mass has been observed and reported in the scientific literature for nearly 2 centuries; however, identification and careful examination of molecular mediators of age-related muscle atrophy have only been possible for roughly 3 decades. Here we review molecular targets of recent interest in age-related muscle atrophy and briefly discuss emerging small molecule therapeutic treatments for muscle wasting in sarcopenic susceptible populations.
引用
收藏
页码:44 / 57
页数:14
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