Fig. 5

The overall acetyl genistin mechanisms related to dexamethasone-induced muscle atrophy. Acetyl genistin exerts its effects on muscle physiology. Acetyl genistin, a potent compound, plays a pivotal role in promoting myoblast differentiation into myotubes by increasing the expression of key markers such as MHC, MyoD, and MyoG. Acetyl genistin encourages myoblast differentiation into myotubes and acts as a natural defense against dexamethasone-induced muscle atrophy. This defense involves the inherent ability of acetyl genistin to regulate AMPK, a pivotal upstream regulator, leading to a subsequent reduction in FoxO1/3 activity and the consequent suppression of MAFbx expression. This dual functionality highlights the potential of acetyl genistin in both facilitating muscle differentiation and protecting against muscle atrophy, contributing to overall muscle health and function. Figure created using Biorender (https://biorender.com/)