| Literature DB >> 32820393 |
Feng Zhu1, Qingyou Meng1, You Yu1, Lianbo Shao2, Zhenya Shen3.
Abstract
Myocardial infarction leads to cardiomyocyte loss, ensuing ventricular pathological remodeling, dramatic impairment of cardiac function, and ultimately heart failure. Unfortunately, the existing therapeutical treatments cannot directly replenish the lost myocytes in the injured myocardium and the long-term prognosis of heart failure after myocardial infarction remains poor. Growing investigations have demonstrated that the adult mammalian cardiomyocytes possess very limited proliferation capacity, and that was not enough to restore the injured heart. Recently, many studies were targeting to promote cardiomyocyte proliferation via inducing cardiomyocyte cell cycle re-entry for cardiac repair after myocardial infarction. Indeed, these results showed it is a feasible way to stimulate terminally differentiated cardiomyocyte proliferation. Here, we reviewed the major mechanisms and the potential targets for stimulating mammalian adult cardiomyocyte proliferation specifically. This will provide a new therapeutic strategy for the clinical treatment of myocardial infarction by activating the endogenous regeneration. Graphical abstract.Entities:
Keywords: Adult cardiomyocyte proliferation; Cell cycle; Extracellular matrix; Myocardial infarction; ncRNA
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Year: 2020 PMID: 32820393 DOI: 10.1007/s12265-020-10067-8
Source DB: PubMed Journal: J Cardiovasc Transl Res ISSN: 1937-5387 Impact factor: 4.132