Targeting necroptosis as therapeutic potential in chronic myocardial infarction.
Chanon PiamsiriChayodom ManeechoteNatthaphat Siri-AngkulSiriporn C ChattipakornSiriporn C ChattipakornPublished in: Journal of biomedical science (2021)
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.
Keyphrases
- randomized controlled trial
- heart failure
- left ventricular
- high glucose
- cell death
- signaling pathway
- cardiovascular disease
- end stage renal disease
- drug induced
- acute heart failure
- ejection fraction
- chronic kidney disease
- diabetic rats
- coronary artery
- magnetic resonance
- type diabetes
- coronary artery disease
- endothelial cells
- prognostic factors
- pi k akt
- peritoneal dialysis
- newly diagnosed
- aortic stenosis
- computed tomography
- patient reported outcomes
- drug delivery
- metabolic syndrome
- cell proliferation
- aortic valve
- adverse drug
- cardiac resynchronization therapy