Id1: a novel therapeutic target for patients with atherosclerotic plaque rupture

Abstract

Plaque neovascularization and inflammation are responsible for plaque destabilization and rupture. However, the precise triggers for inflammation and neovascularization in atherosclerosis are largely unknown. Id1 (inhibitor of DNA-binding) protein is a helix-loop-helix transcription factor and plays an important role in angiogenesis and inflammation. The expression of Id1 can be up-regulated by plaque formation factors such as vascular endothelial growth factor (VEGF), hypoxia, NAD(P)H oxidase, and TNF-alpha. Moreover, Id1 is critical to endothelial progenitor cell (EPC) population formation and angiogenesis. Evidence from diverse sources has suggested that Id1 may affect plaque destabilization through angiogenesis and inflammation. Herein we hypothesize that Id1 is an important protein for the development and progression of atherosclerotic plaque destabilization and hence blocking the expression of Id1 may serve as new targets for antiatherogenic therapy.