This work is devoted to the thermodynamic and electrochemical processes occurring in the life cycle of mitochondria, which determine the functional activity of any cell, be it immune cells or vascular endothelium. During atherogenesis, resident cells of the immune system (monocytes), once in the subendothelial space, differentiate into M1 type macrophages, which initiate an inflammatory response. Mitochondria in type M1 macrophages not only produce specific pro-inflammatory proteins, but first of all acidify the phagosome environment with hydrogen cations (H+) and reactive oxygen species (ROS) as quickly as possible, as well as increase heat production, which contributes to the most effective phagocytosis of the pathogen . At the same time, the mitochondrial network is split into many small isolated fragments (fission), which maximizes the area of the outer membrane (10-15 times) and, accordingly, increases the rate of heat transfer. For this purpose, the electrochemical potential (??m) is uncoupled on the inner membrane, which under physiological conditions is carried out either by fatty acids or by thermochemical accumulation of Ca2+ and Pi cations in the matrix in the form of calcium phosphate (CaP). With a long stay of mitochondria in this thermodynamic regime, macrophages of the M1 type accumulate lipids, transform into "foamy" cells, and amorphous CaP, capable of crystallization. A functional imbalance of the mitochondrial acid-base state and redox status in M1 macrophages, caused by a long-term energy restructuring to anaerobic glycolysis, also contributes to the pro-inflammatory immune response. In this case, there is a chronic imbalance in the production of hydrogen cations (H+) and ROS, the value of which gradually begins to exceed the level allowed by the backlash of functionality, which in turn further potentiates inflammation, mtDNA damage, hyperlipidemia, with the final formation of CaP salts. In the context of atherosclerosis, mitophagy can reduce the inflammatory response caused by M1 macrophages, reduce the degradation of endothelial cells, however, with the loss of metabolic flexibility of the dissimilation process, mitophagy is not completely completed, which leads to overflow of cells with degraded organelles, which are overloaded with CaP agglomerates.

Tatevosyan Artur defended his doctoral thesis in 2000 at the Research Institute of Urology in Moscow on the pathogenesis of kidney stone disease. Currently Professor at the Department of Urology at Kuban State Medical University. In recent years, scientific interests have been associated with the study of thermodynamic and electrochemical processes occurring in mitochondria (Mx), since it is the dysfunction of mitochondria that is the cause of the development of both aseptic inflammation in the tissues of various organs and systems, and their subsequent pathological calcification. I am responsible for the departmental research work "EVALUATION OF ENERGY METABOLISM FOR THE PREVENTION AND TREATMENT OF COMORBID DISEASES". Participated in more than 50 different conferences, published more than 80 articles, received 2 copyright certificates for inventions and 5 patents. I am a member of the editorial boards of several journals.