骨骼肌
Wnt信号通路
下调和上调
间歇性缺氧
体内
肌肉萎缩
内分泌学
连环素
内科学
缺氧(环境)
心肌细胞
医学
化学
生物
信号转导
细胞生物学
生物化学
有机化学
生物技术
氧气
阻塞性睡眠呼吸暂停
基因
作者
Hua Guo,Yunyun Zhang,Tingting Han,Xiaochuan Cui,Xiang Lü
标识
DOI:10.1016/j.archger.2021.104460
摘要
Sleep breathing disorder may affect skeletal muscle decline in the elderly, but the mechanism is not clear. Therefore, this study explores the mechanism of skeletal muscle aging in chronic intermittent hypoxia (CIH) rats. In vitro and in vivo CIH models were constructed in L6 cells and SD rats by treating chronic intermittent hypoxia. Pathological changes of skeletal muscle in vivo were measured by hematoxylin-eosin (HE) staining. Cell proliferation and apoptosis were detected by CCK-8 and Flow cytometer, respectively. The expression of KLC1/GRX1 and the proteins related to the Wnt/β-catenin pathway were measured by qRT-PCR and western blot. CIH model was successfully established induced by chronic intermittent hypoxia with lower skeletal muscle index (SMI), increased inward migration of muscle fiber cell nucleus, and muscle cells’ distance. The results showed that Wnt/β-catenin signalling was activatedin both L6 cells and CIH rats’ model. KLC1 and GRX1 were significantly downregulated in the CIH model. Loss of function showed that downregulation of KLC1 promoted L6 cell and skeletal muscle aging in vitro and in vivo, respectively. Our results demonstrated that CIH aggravated skeletal muscle aging by down-regulating KLC1/GRX1 expression via the Wnt/β-catenin pathway.
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