Rapamycin promotes vascular smooth muscle cell differentiation through insulin receptor substrate-1/phosphatidylinositol 3-kinase/Akt2 feedback signaling
The phenotypic plasticity of mature vascular smooth muscle cells (VSMCs) facilitates
angiogenesis and wound healing, but VSCM dedifferentiation also contributes to vascular
pathologies such as intimal hyperplasia. Insulin/insulin-like growth factor I (IGF-I) is unique
among growth factors in promoting VSMC differentiation via preferential activation of
phosphatidylinositol 3-kinase (PI3K) and Akt. We have previously reported that rapamycin
promotes VSMC differentiation by inhibiting the mammalian target of rapamycin (mTOR) …
angiogenesis and wound healing, but VSCM dedifferentiation also contributes to vascular
pathologies such as intimal hyperplasia. Insulin/insulin-like growth factor I (IGF-I) is unique
among growth factors in promoting VSMC differentiation via preferential activation of
phosphatidylinositol 3-kinase (PI3K) and Akt. We have previously reported that rapamycin
promotes VSMC differentiation by inhibiting the mammalian target of rapamycin (mTOR) …