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Targeting Necroptosis As Therapeutic Potential in Chronic Myocardial Infarction

Overview
Journal J Biomed Sci
Publisher Biomed Central
Specialty Biology
Date 2021 Apr 10
PMID 33836761
Citations 19
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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.

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References
1.
Hu X, Chen X, Pang H, Liu H, Chen P, Shi J . Plasma levels of receptor interacting protein kinase-3 correlated with coronary artery disease. Chin Med J (Engl). 2019; 132(12):1400-1405. PMC: 6629337. DOI: 10.1097/CM9.0000000000000225. View

2.
Negroni A, Colantoni E, Cucchiara S, Stronati L . Necroptosis in Intestinal Inflammation and Cancer: New Concepts and Therapeutic Perspectives. Biomolecules. 2020; 10(10). PMC: 7599789. DOI: 10.3390/biom10101431. View

3.
Lau A, Wang S, Jiang J, Haig A, Pavlosky A, Linkermann A . RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival. Am J Transplant. 2013; 13(11):2805-18. DOI: 10.1111/ajt.12447. View

4.
Liu J, Wu P, Wang H, Wang Y, Du Y, Cheng W . Necroptosis Induced by Ad-HGF Activates Endogenous C-Kit+ Cardiac Stem Cells and Promotes Cardiomyocyte Proliferation and Angiogenesis in the Infarcted Aged Heart. Cell Physiol Biochem. 2016; 40(5):847-860. DOI: 10.1159/000453144. View

5.
Gan I, Jiang J, Lian D, Huang X, Fuhrmann B, Liu W . Mitochondrial permeability regulates cardiac endothelial cell necroptosis and cardiac allograft rejection. Am J Transplant. 2018; 19(3):686-698. DOI: 10.1111/ajt.15112. View