BCL2-regulated apoptotic process in myocardial ischemia-reperfusion injury (Review)
| Autor: | S. P. Syatkin, Anna Yu. Korshunova, Enzo Agostinelli, Said M. Semyatov, Anastasia P. Sklifasovskaya, M. L. Blagonravov, E.V. Neborak |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Programmed cell death BCL2 MAP Kinase Signaling System Ischemia Muscle Proteins Myocardial Reperfusion Injury myocardial ischemia-reperfusion injury 03 medical and health sciences 0302 clinical medicine cardioprotective therapy Genetics medicine Humans Protein kinase B PI3K/AKT/mTOR pathway Cause of death business.industry Myocardium Intrinsic apoptosis apoptosis regulated cell death General Medicine Articles medicine.disease 030104 developmental biology Proto-Oncogene Proteins c-bcl-2 Apoptosis 030220 oncology & carcinogenesis Cancer research business Reperfusion injury |
| Zdroj: | International Journal of Molecular Medicine |
| ISSN: | 1791-244X 1107-3756 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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