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Electron microscopy of the studied samples. Probably, the "classic" apoptotic cell degradation was rarely observed and/or it occurred transiently. Usually apoptous cills - fragments of the dead cell disappear without a trace in an average of 90 minutes. They are phagocytized by macrophages or neighbouring cells without the development of an inflammatory reaction. The morphologically recorded process of apoptosis lasts 1-3 hours.

Recently, apoptosis has attracted the attention of cardiologists as a potential pathogenetic factor not only of progressive chronic heart failure, but also of many other forms of pathology of the cardiovascular system: coronary atherosclerosis, myocardial infarction, large-focal post-infarction cardiosclerosis, cardiomyopathies, etc. To study the participation of apoptosis in the death of cardiomyocytes, the hearts of those who died from cardiovascular forms of pathology are studied. In addition, induced apoptosis of cardiomyocytes in experimental animals (rats, rabbits, dogs) is widely studied in the conditions of modelling such forms of pathology.

Before analysing the participation of apotosis in the death of cardiomyocytes, let's consider modern ideas about apoptosis. Currently, it is believed that apoptosis is a polyetiological process, since it is induced by a variety of factors and, at the same time, it is obviously monopathogenetic, i.e. in general it develops according to a single scenario, regardless of the nature of the cause that caused it. Polyetiology and monopathogeneticity are the main criteria of any typical pathological process. Apoptosis is an evolutionarily developed process, i.e. essentially a Defence-adaptive process. All such processes can acquire a pathogenic character under certain, specific conditions of their occurrence and development. Biologically active substances involved in the regulation of apoptosis are usually proteins, and their synthesis is controlled by the corresponding genes. Genes that stimulate apoptosis include genes p53, Vach, Bcl-xS. At the same time, genes that program protein synthesis are known - in-

Apoptosis inhibitors (Bc1-2, Ced-9, MCL-1 - induced Myeloid Leukaemia Cell

Differentiation protein; MCL-1 is the same protein that is called the "survival factor", as it prolongs the life of cells). The most striking and informative proteins reflecting proliferative processes in cells and tissues are the proteins of the Vs1-2 family (they are classified as G-proteins), which occupy a central place in the regulation of apoptosis. To date, it is known that some proteins of the Bc1-2 family are inducers of apoptosis (Bad, Bax, J3ik, Bid, Bak), and others are its inhibitors (Bcl-2, Bcl-X). Pro- and anti-apoptosis proteins are able to combine with each other, forming homo- and heterodimers.) For example, when combining the apoptosis inhibitor of the Vsl-2 protein with the Apoptosis activator protein Vach, the total effect, i.e. inhibition or activation of apoptosis, will be determined by which protein will prevail in this complex.

Apoptosis plays an important role in the morphogenesis of the body, being a "instrument" for maintaining homeostatic balance between processes.                                 Explainn