APOPTOSIS IN ATHEROGENESIS - IMPLICATIONS FOR PLAQUE DESTABILIZATION

Atherosclerotic plaques in coronary arteries are composed of a crescen t-shaped mass of lipids separated from the lumen by a fibrous cap. Los s of smooth muscle cells (SMCs) in the fibrous cap could have serious consequences, since SMCs ale the only cells in the cap that can synthe size collagen fibres types I and III. These fibres maintain the tensil e strength of the fibrous cap. The role of cell loss and apoptotic cel l death in the progression of atherosclerosis has received renewed att ention recently in the literature. The large variability in the report ed values for the percentage of apoptotic cells in plaques can be expl ained by the aspecificity of the TUNEL technique used to detect apopto sis. Despite this variability, there is no doubt that both SMCs and ma crophages can die in plaques through apoptosis. The significance of ma crophage apoptosis is very different from that of SMC apoptosis. Incre ased apoptosis of SMCs in the vulnerable regions of the plaque can res ult in weakening of the fibrous cap, whereas increased macrophage apop tosis can lead to plaque stabilization through decreased breakdown of collagen. Cytoplasmic remnants of apoptotic SMCs often remain in the p laque as matrix vesicles. These small calcium-containing vesicles coul d initiate plaque calcification.