Apoptosis in atheroclerosis: implications for plaque destabilization.

An increasing body of evidence from both animal models and human specimens suggests that apoptosis or programmed cell death is a major event in the pathophysiology of atherosclerosis. Although the significance of apoptosis in atherosclerosis remains unclear, it has been proposed that apoptotic cell death contributes to plaque instability, rupture and thrombus formation. In this study, we have outlined some of our most recent results concerning initiation of apoptosis in atherosclerosis with a special focus on oxidative DNA and RNA damage. Furthermore, we provide a detailed picture of the pro- and anti-apoptotic genes/proteins that are involved during the initiation of cell death in atherosclerotic plaques by using a combination of established immunohistochemical stainings and recent molecular biology techniques. Our data suggest that smooth muscle cells and macrophages in atherosclerotic plaques express a different panel of apoptosis-related genes in response to proapoptotic stimuli. Although this may seem a promising starting-point for the development of anti-atherogenic drugs, it remains to be determined whether modulation of apoptosis can become a clinically important approach to influence plaque progression.