Apoptosis in atherosclerosis: pathological and pharmacological implications.

Normal embryonic development, tissue differentiation and repair in the eukaryote requires a tightly regulated apoptosis, or programmed cell death. Apoptosis also plays an essential role in different pathological processes including atherosclerosis, in which it affects all cell types in the atherosclerotic lesion, including endothelial cells, vascular smooth muscle cells, and macrophages. During atherosclerosis progression, pro- and anti-apoptotic signals abound in the evolving lesion. Apoptosis limits the number of a particular cell type that accumulates in the lesion and slows down the overall progression of the lesion. On the other hand, it contributes to the production of unstable plaques. Many pharmacological agents used to treat cardiovascular and lipid disorders have pro- or/and anti-apoptotic effects. Pharmaceuticals that modulate apoptosis in specific types of cell can potentially serve as anti-atherogenic agents. However, to develop agents for clinical use requires a thorough knowledge of the pathophysiology of apoptosis in atheromatous lesions, a highly cell-specific process. Here we review our current understanding of the process to provide a background for future pharmacological research in the area.