Regular aerobic exercise can effectively ameliorate the skeletal muscle and mitochondrial function impairments caused by bves deficiency in zebrafish

Skeletal muscles of patients with the homozygous missense variant of Bves exhibit impaired membrane trafficking, while skeletal muscle fibers in bvesS191F homozygous mutant zebrafish are significantly reduced and disorganized.

However, the mechanism by which the absence of bves induces skeletal muscle atrophy remains unclear. In this study, we discovered a novel mechanism whereby Bves deficiency drives skeletal muscle atrophy by disrupting mitochondrial structure and function. Our findings indicate that bves knockout leads to a significant decrease in the swimming ability of zebrafish, atrophy of skeletal muscle tissue, loss of cell membrane localization signals, and abnormalities in mitochondrial structure and function.