Initiation of angiogenesis in atherosclerosis: smooth muscle cells as mediators of the angiogenic response to atheroma formation.

Neovascularization of atherosclerotic lesions favors their progression toward rupture. Despite this pathophysiological importance, data regarding the mechanism(s) initiating plaque neovascularization are scarce. Recent findings indicate that smooth muscle cells located underneath early aortic atheromatous lesions display a pro-angiogenic phenotype, and that lipid mediators derived from these lesions are potent inducers of this phenotypic change. Here, we discuss these new data suggesting that smooth muscle cells could be the central organizers of an angiogenic response initiated by the very first cause of the atheromatous disease, the accumulation and retention of lipids in the arterial wall.