Inhibition of vascular intimal hyperplasia by the myokine Musclin: the role of NPR3/raptor/mTORC1-mediated glycolysis and phenotypic switching of VSMCs

• Musclin overexpression in skeletal muscle reduces injury-induced vascular intimal hyperplasia in mice. • Musclin inhibits PDGF-BB-induced VSMC proliferation, migration, and glycolysis while promoting differentiation marker expression. • Mechanistically, Musclin suppresses mTORC1 activity via NPR3-raptor interaction, which is essential for its effects on VSMC phenotypic switching. • Restoring mTORC1 activity or silencing NPR3 abolishes Musclin's protective effects, highlighting potential therapeutic targets for vascular restenosis.