Fig. 8
Putative mechanistic map of the mechanisms by which aerobic exercise resists sarcopenia through the miR-128/IGF-1 signaling pathway. d-galactose (d-gal) contributes to the development of sarcopenia by causing metabolic disturbances in vivo to produce large amounts of reactive oxygen species (ROS) and promote the expression of muscle atrophy-related factors MuRF1, Atrogin1, and miR-128. Aerobic exercise inhibits miR-128 expression, which activates the expression of its direct target, insulin-like growth factor-1 (IGF-1). IGF-1 may further promote phosphorylation of FOXO3a by activating PI3K/AKT and PGC1-? signaling pathways. These changes may improve mitochondrial function impaired by d-gal induction, thereby resisting sarcopenia. ATP, adenosine triphosphate; ADP, adenosine diphosphate; SOD, superoxide dismutase. |