浪费的
骨骼肌
萎缩
合成代谢
平衡
心力衰竭
再生(生物学)
心肌细胞
肌肉萎缩
肌萎缩
自噬
内科学
肌肉无力
肌肉肥大
内分泌学
弱点
医学
生物
细胞生物学
解剖
生物化学
细胞凋亡
作者
Harrison Gallagher,Paul W. Hendrickse,Marcelo G. Pereira,T. Scott Bowen
标识
DOI:10.1016/j.jshs.2023.04.001
摘要
This review highlights some established and some more contemporary mechanisms responsible for heart failure (HF)-induced skeletal muscle wasting and weakness. We first describe the effects of HF on the relationship between protein synthesis and degradation rates, which determine muscle mass, the involvement of the satellite cells for continual muscle regeneration, and changes in myofiber calcium homeostasis linked to contractile dysfunction. We then highlight key mechanistic effects of both aerobic and resistance exercise training on skeletal muscle in HF and outline its application as a beneficial treatment. Overall, HF causes multiple impairments related to autophagy, anabolic-catabolic signaling, satellite cell proliferation, and calcium homeostasis, which together promote fiber atrophy, contractile dysfunction, and impaired regeneration. Although both wasting and weakness are partly rescued by aerobic and resistance exercise training in HF, the effects of satellite cell dynamics remain poorly explored.
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