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Targeting necroptosis as therapeutic potential in chronic myocardial infarction
Chanon Piamsiri1,2,3, Chayodom Maneechote1,3, Natthaphat Siri-Angkul1,2,3
1Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Insights
Necroptosis, a cell death pathway, plays a role in heart failure after myocardial infarction (MI). Inhibiting necroptosis may improve cardiac function and viability in chronic MI patients.
Area of Science:
- Cardiology
- Molecular Biology
- Pathology
Background:
- Cardiovascular diseases (CVDs) are the leading global cause of death, with myocardial infarction (MI) being the most common type.
- MI leads to cardiomyocyte death, adverse cardiac remodeling, and heart failure (HF).
- Necroptosis is implicated in cardiomyocyte loss during MI-induced HF, though mechanisms are not fully understood.
Purpose of the Study:
- To comprehensively review the mechanisms of necroptosis in chronic MI-induced heart failure.
- To synthesize findings from in vitro, in vivo, and clinical studies.
- To identify potential therapeutic targets for improving outcomes in MI patients.
Main Methods:
- Literature review of in vitro, in vivo, and clinical studies on necroptosis in MI-induced HF.
- Analysis of the role of necroptosis signaling pathways in cardiac remodeling and dysfunction.
- Evaluation of the therapeutic potential of necroptosis inhibitors.
Main Results:
- Necroptosis contributes to cardiomyocyte loss and cardiac dysfunction following MI.
- Recent studies suggest necroptosis inhibitors can improve cell viability and cardiac function in chronic MI models.
- The precise mechanisms linking necroptosis to HF progression require further elucidation.
Conclusions:
- Understanding necroptosis mechanisms is crucial for developing novel therapeutic strategies for MI-induced HF.
- Targeting necroptosis pathways holds promise for improving clinical outcomes in patients with chronic heart failure post-MI.
Abstract:
Cardiovascular diseases (CVDs) are considered the predominant cause of morbidity and mortality globally. Of these, myocardial infarction (MI) is the most common cause of CVD mortality. MI is a life-threatening condition which occurs when coronary perfusion is interrupted leading to cardiomyocyte death. Subsequent to MI, consequences include adverse cardiac remodeling and cardiac dysfunction mainly contribute to the development of heart failure (HF). It has been shown that loss of functional cardiomyocytes in MI-induced HF are associated with several cell death pathways, in particular necroptosis. Although the entire mechanism underlying necroptosis in MI progression is still not widely recognized, some recent studies have reported beneficial effects of necroptosis inhibitors on cell viability and cardiac function in chronic MI models. Therefore, extensive investigation into the necroptosis signaling pathway is indicated for further study. This article comprehensively reviews the context of the underlying mechanisms of necroptosis in chronic MI-induced HF in in vitro, in vivo and clinical studies. These findings could inform ways of developing novel therapeutic strategies to improve the clinical outcomes in MI patients from this point forward.
