Apoptotic cell death in atherosclerosis.
OBJECTIVE
Apoptosis is a critical regulator of homeostasis in many tissues, including the vasculature. Apoptosis in atherosclerotic lesions is triggered by inflammatory processes, both via cell-cell contact and by cytokines and oxidized lipids. Apoptosis of vascular smooth muscle cells, endothelial cells and macrophages may promote plaque growth and pro-coagulation and may induce rupture, the major consequence of atherosclerosis in humans.


RESULTS
Studies over the past year have clearly demonstrated the significance of cell death in atherosclerosis. Some of the key cellular, cytokine and molecular regulators that contribute to the apoptosis of cells within the atherosclerotic lesion have been identified and their mechanism of action elucidated. Other studies have shed some light on the identity of cells whose loss by apoptosis contributes to plaque instability.


CONCLUSIONS
The identification of which cell types undergo apoptosis within the atherosclerotic lesion, the extracellular factors that impinge on these cells, and the intracellular mechanisms that govern their demise have begun to be elucidated. This information is critical in the design of further in-vivo experiments such as the exploitation of animal models, and ultimately, in applying this knowledge to clinical practice.
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001161:Arteriosclerosis / Q000378:metabolism / Q000503:physiopathology*; D001808:Blood Vessels / Q000503:physiopathology; D042783:Endothelial Cells / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008264:Macrophages / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology