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BCL2‑regulated apoptotic process in myocardial ischemia‑reperfusion injury (Review)
Anna Yu Korshunova1, Mikhail L Blagonravov1, Ekaterina V Neborak2
1Department of Pathophysiology, Peoples' Friendship University of Russia (RUDN University), 117198 Moscow, Russian Federation.
Insights
Cardiovascular disease causes many deaths. Myocardial ischemia-reperfusion injury (MI/RI) can be treated by targeting BCL2-regulated apoptosis, a key mechanism in saving heart cells after heart attacks.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Death Research
Background:
- Cardiovascular disease is a leading cause of death globally.
- Myocardial ischemia-reperfusion injury (MI/RI) is a significant complication following treatment for heart attacks.
- Understanding regulated cell death mechanisms, like apoptosis, is crucial for developing cardioprotective therapies.
Purpose of the Study:
- To review the mechanisms of BCL2-regulated apoptosis in the context of MI/RI.
- To identify potential therapeutic targets for cardioprotection.
- To explore strategies for saving viable cardiomyocytes after MI/RI.
Main Methods:
- Review of existing scientific literature on BCL2, apoptosis, and MI/RI.
- Analysis of signaling pathways regulating BCL2, including PI3K/AKT, MEK1/ERK1/2, and JAK2/STAT3.
- Examination of other regulatory factors such as endothelial nitric oxide synthase, PTEN, cardiac ankyrin repeat protein, and microRNA.
Main Results:
- BCL2 is a critical anti-apoptotic protein in the myocardium.
- Dysregulation of BCL2 contributes to cardiomyocyte death during MI/RI.
- Several signaling pathways and molecules modulate BCL2 activity and represent therapeutic targets.
Conclusions:
- Targeting BCL2-regulated apoptosis offers a promising strategy for treating MI/RI.
- Inhibiting intrinsic apoptosis can preserve viable cardiomyocytes and improve outcomes after MI/RI.
- Further research into these pathways may lead to novel cardioprotective therapies.
Abstract:
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.
