Altered mitochondrial function is currently recognized as an important factor in atherosclerosis initiation and progression. Mitochondrial dysfunction can be caused by mitochondrial DNA (mtDNA) mutations, which can be inherited or spontaneously acquired in various organs and tissues, having more or less profound effects depending on the tissue energy status. Arterial wall cells are among the most vulnerable to mitochondrial dysfunction due to their barrier and metabolic functions. In atherosclerosis, mitochondria cause alteration of cellular metabolism and respiration and are known to produce excessive amounts of reactive oxygen species (ROS) resulting in oxidative stress. These processes are involved in vascular disease and chronic inflammation associated with atherosclerosis. Currently, the list of known mtDNA mutations associated with human pathologies is growing, and many of the identified mtDNA variants are being tested as disease markers. Alleviation of oxidative stress and inflammation appears to be promising for atherosclerosis treatment. In this review, we discuss the role of mitochondrial dysfunction in atherosclerosis development, focusing on the key cell types of the arterial wall involved in the pathological processes. Accumulation of mtDNA mutations in isolated arterial wall cells, such as endothelial cells, may contribute to the development of local inflammatory process that helps explaining the focal distribution of atherosclerotic plaques on the arterial wall surface. We also discuss antioxidant and anti-inflammatory approaches that can potentially reduce the impact of mitochondrial dysfunction.

Changes in the level of blood cell-free circulating mitochondrial DNA were examined during experimental adrenaline-induced myocardial injury in rats. The amount of mitochondrial DNA in the blood was significantly elevated at 48 and 72 h after subcutaneous injection of adrenaline solution, and it was accompanied by development of multiple small-focal myocardial ischemia. This suggests that the measured level of blood cell-free circulating mitochondrial DNA might be used as a biomarker of acute myocardial ischemia.

The aim of the present investigation is to study the level of plasma mtDNA as a potential marker of cardiomyocyte damage in 2 and 4 h after subcutaneous injection of adrenaline and during the formed morphological alterations of the myocardium (3 days). Methods. Real time PCR. Male Wistar rats were used as the experimental animals. Results. It was shown that during the increase in the activity of cytolysis biomarkers, at the first hours after adrenaline injection, no reliable increase is observed in the level of free circulating blood mtDNA. A tendency of 2.5-fold increase in this parameter was established at the third day after adrenaline injection during the development of acute inflammatory process in the myocardium. On the whole, further researches are needed on the dynamics of mtDNA level upon acute damage of the myocardium in experimental and clinical investigations for unbiased estimation of the prospects of using the parameter in laboratory diagnostics

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