Reactive oxygen species in the pathogenesis of sarcopenia☆

被引:11
作者
Xu, Hongyang [1 ]
Brown, Jacob L. [1 ,2 ]
Bhaskaran, Shylesh [1 ]
Van Remmen, Holly [1 ,2 ]
机构
[1] Oklahoma Med Res Fdn, Aging & Metab Res Program, Oklahoma City, OK 73104 USA
[2] Oklahoma City VA Med Ctr, Oklahoma City, OK 73104 USA
关键词
Aging; Sarcopenia; Mitochondria; Neuromuscular junction; Skeletal muscle; SKELETAL-MUSCLE FIBERS; HYDROPEROXIDE GLUTATHIONE-PEROXIDASE; CUZN-SUPEROXIDE-DISMUTASE; FREE-RADICAL GENERATION; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; CONTRACTILE PROPERTIES; S-GLUTATHIONYLATION;
D O I
10.1016/j.freeradbiomed.2024.11.046
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
One of the most critical factors impacting healthspan in the elderly is the loss of muscle mass and function, clinically referred to as sarcopenia. Muscle atrophy and weakness lead to loss of mobility, increased risk of injury, metabolic changes and loss of independence. Thus, defining the underlying mechanisms of sarcopenia is imperative to enable the development of effective interventions to preserve muscle function and quality in the elderly and improve healthspan. Over the past few decades, understanding the roles of mitochondrial dysfunction and oxidative stress has been a major focus of studies seeking to reveal critical molecular pathways impacted during aging. In this review, we will highlight how oxidative stress might contribute to sarcopenia by discussing the impact of oxidative stress on the loss of innervation and alteration in the neuromuscular junction (NMJ), on muscle mitochondrial function and atrophy pathways, and finally on muscle contractile function.
引用
收藏
页码:446 / 458
页数:13
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