Abstract
Cardiovascular disease has been, and remains, one of the leading causes of death in the modern world. The elderly are a particularly vulnerable group. The aging of the body is inevitably accompanied by the aging of all its systems, and the cardiovascular system is no exception. The aging of the cardiovascular system is a significant risk factor for the development of various diseases and pathologies, from atherosclerosis to ischemic stroke. Mitochondria, being the main supplier of energy necessary for the normal functioning of cells, play an important role in the proper functioning of the cardiovascular system. The functioning of each individual cell and the organism as a whole depends on their number, structure, and performance, as well as the correct operation of the system in removing non-functional mitochondria. In this review, we examine the role of mitochondria in the aging of the cardiovascular system, as well as in diseases (for example, atherosclerosis and ischemic stroke). We pay special attention to changes in mitochondrial dynamics since the shift in the balance between fission and fusion is one of the main factors associated with various cardiovascular pathologies.
Highlights
Mitochondria are the a main energetic organelles of the cell
Violations of the composition of phospholipids can alter numerous mitochondrial characteristics, including membrane integrity, fluidity, and permeability. This results in problems in the stability and activity of several proteins associated with the inner membrane, including those involved in electron transport chains and oxidative phosphorylation [4]
Maintaining the balance between mitochondrial fission and fusion could be a more promising strategy to delay cardiac abnormalities related to aging than stimulating or suppressing one of these mechanisms
Summary
Mitochondria are the a main energetic organelles of the cell. They are responsible for the production of the main part of the energy utilized for cells’ metabolism. Violations of the composition of phospholipids can alter numerous mitochondrial characteristics, including membrane integrity, fluidity, and permeability This results in problems in the stability and activity of several proteins associated with the inner membrane, including those involved in electron transport chains and oxidative phosphorylation [4]. Numerous human diseases, including cardiovascular pathologies, are based, at least in part, on mitochondrial dysfunction This dysfunction leads to oxidative stress, which arises from the over-production of reactive oxygen species (ROS) by the mitochondria as by-products of the respiratory chain functioning [5]. Today’s knowledge suggests that mitochondria are derived from prokaryotic endosymbionts This hypothesis is supported by the fact that they share a certain degree of autonomy and some characteristic features of bacteria [7]. Mutations of mtDNA are usually described at the heteroplasmy level or as a percentage of mutant copies per genome [4]
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