Chronic intermittent hypoxia aggravates skeletal muscle aging by down-regulating Klc1/grx1 expression via Wnt/β-catenin pathway

•Wnt/β-catenin signalling pathway was activated in CIH model.•The expressions of KLC1 and GRX1 were significantly downregulated in CIH model.•Wnt/β-catenin signalling was activated and KLC1/GRX1 was inhibited in L6 cells with chronic intermittent hypoxia treatment.•Downregulation of KLC1 promoted L6 cell and skeletal muscle aging. 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.