Matrine suppresses advanced glycation end products-induced human coronary smooth muscle cells phenotype conversion by regulating endoplasmic reticulum stress-dependent Notch signaling.

Abstract excerpt

Advanced glycation end products (AGEs) induce vascular smooth muscle cells (VSMCs) contractile-synthetic phenotypic conversion which plays roles in aggravated atherosclerosis in diabetes. Matrine has been proved to suppress AGEs-induced phenotypic conversion which is governed by Notch pathway. Endoplasmic reticulum stress was associated with Notch pathway. Cultured human coronary smooth muscle cells (HCSMCs) were...

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