Apelin is a peptide increasing tolerance of organs and cells to ischemia and reperfusion. The molecular mechanism (the review)

Ischemic-reperfusion injuries of organs underlie such common pathologies as ischemic stroke and myocardial infarction and are the cause of death and disability in the population. In addition, ischemic lung damage is observed in pulmonary embolism. Advances in transplantology, as well as the widespread use of coronary artery bypass grafting, raise the problem of ischemia and reperfusion of organs during these manipulations. Progress made over the past three decades in the treatment of stroke and acute myocardial infarction (AMI) has slowed in recent years. Since patients with stroke and AMI are admitted to the hospital with ischemic damage to the brain or heart, it is no longer possible to influence its formation. However, it is possible to affect reperfusion injury to organs. Significant progress in improving the efficiency of kidney transplantation, in the treatment of stroke, pulmonary embolism and AMI can be achieved through the development of new drugs that can effectively prevent reperfusion damage of organs. Synthetic analogues of apelin with a long half-life can become prototypes of drugs with similar action. It has been found that apelins can increase the tolerance of the heart, brain, kidneys and lungs to ischemia/reperfusion (I/R). Apelins inhibit apoptosis and activate cardiomyocyte autophagy. The neuroprotective, cardioprotective, renoprotective, and pulmonoprotective effects of apelins are realized through intracellular signaling, including protein kinases, a mitochondrial variable permeability pore, and ATP-sensitive K+ channels. Enzyme-resistant analogues of apelin are promising peptides for the treatment of AMI, stroke, and I/R damage to the lungs, and kidneys.