[Role of apoptosis in the pathogenesis of atherosclerosis]

The recent information about importance of programmed cell death in the development of atherosclerosis was reviewed. It was emphasized, that intensiveness of apoptosis was various for smooth muscle cells, macrophages, endothelial cells, lymphocytes, and changed during the development of such a multistage process as atherosclerosis. Is was proved, that exactly apoptosis gave specific features to the atherosclerotic process. The agents inducing atherosclerosis (modified lipoprotein, mechanical influences, viruses, bacterial toxins, etc.), have insufficient for initiation of necrosis. The damage to vascular wall in atherosclerosis is characterized not by intensive influence of pathogenic factors, but rather constant chronic influence of the agents of moderate power. Therefore, it is just apoptosis that makes up the critical mechanism of the reactive-regeneration answer of vascular wall structures to an injure. Evolutionally, the apoptic way of the development of answer to an injure appears to be more rational, as for as it results in minimal losses of cells due to both secondary alteration and maintenance of fast restoration of the primary cellular architecture of injured tissues at the expense of the natural mechanisms of regulation of apoptosis and proliferation. In the certain situation, these positive aspects of apoptosis make up a basis for the development of a pathology--failures in the program of apoptosis result in chronic proliferative-degenerative processes, that is in atherosclerosis.