Galangin inhibits neointima formation induced by vascular injury <i>via</i> regulating the PI3K/AKT/mTOR pathway
Bing Wu, Changwu Xu, Hua‐Sheng Ding, Liqiang Qiu, Jixian Gao, Ming Li, Yuanguo Xiong, Hao Xia, Xiaoxiong Liu
Abstract
: Our study suggests that galangin inhibits neointimal hyperplasia after vascular injury by inhibiting smooth muscle cell proliferation, migration and phenotypic switching and by promoting autophagy, and that galangin may be a promising drug for the prevention and treatment of vascular restenosis after PCI.
Topics & Concepts
GalanginNeointimaPI3K/AKT/mTOR pathwayVascular smooth muscleProtein kinase BNeointimal hyperplasiaBlotChemistryPharmacologyCell biologyPhenotypic switchingMedicineSignal transductionBiologyInternal medicineBiochemistryRestenosisStentAntioxidantSmooth muscleKaempferolGeneQuercetinBioactive Natural Diterpenoids ResearchAutophagy in Disease and Therapy