Open AccessBCL2‑regulated apoptotic process in myocardial ischemia‑reperfusion injury (Review)
Author(s) -
A Yu Korshunova,
М. Л. Благонравов,
Е. В. Неборак,
S. P. Syatkin,
A. P. Sklifasovskaya,
S M Semyatov,
Enzo Agostinelli
Publication year - 2020
Publication title -
international journal of molecular medicine
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2020.4781
Subject(s) - apoptosis , reperfusion injury , ischemia , programmed cell death , medicine , pi3k/akt/mtor pathway , protein kinase b , pharmacology , cancer research , microbiology and biotechnology , cardiology , biology , biochemistry
The leading cause of death in developed countries is cardiovascular disease, where coronary heart disease is the main cause of death. Myocardial reperfusion is the most significant method to prevent cell death after ischemia. However, restoration of blood flow may paradoxically lead to myocardial ischemia‑reperfusion injury (MI/RI) accompanied by metabolic disturbances and cardiomyocyte death. As the myocardium has an extremely limited ability to regenerate, the mechanisms of regulated cell death, including apoptosis, are the most significant for contemporary research due to their reversibility. BCL2 is a key anti‑apoptotic protein. There are several signaling pathways and compounds regulating BCL2, including PI3K/AKT and MEK1/ERK1/2, JAK2/STAT3, endothelial nitric oxide synthase, PTEN, cardiac ankyrin repeat protein and microRNA, which can serve as targets for modern methods of cardioprotective therapy inhibiting intrinsic apoptosis and saving viable cardiomyocytes after MI/RI. The present review considers the mechanisms of Bcl2‑regulated apoptosis in the development and treatment of MI/RI.