Unexpected proatherogenic properties of p21: beyond cell cycle control?

Atherosclerosis is an inflammatory disease that involves the interplay between endothelial cells, smooth muscle cells (SMCs), and immune cells.1,2 Various atherogenic stimuli lead to endothelial damage, which in turn triggers the adhesion and extravasation of circulating monocytes and lymphocytes into the artery wall. Resident immune cells produce a plethora of inflammatory mediators that exacerbate leukocyte recruitment and proliferation and promote SMC growth and migration from the underlying media toward the developing atheroma. Abnormal cell proliferation and migration are also a hallmark of neointimal thickening during postangioplasty restenosis, transplant vasculopathy, and graft atherosclerosis.1,3