Key result
Silencing of Rb1 and Meis2 in adult cardiomyocytes resulted in marked cardiomyocyte proliferation, reduced infarct size, and improved cardiac function post-myocardial infarction.
Why the study?
Adult mammalian cardiomyocytes are principally nonproliferative, so augmented proliferation of preexisting cardiomyocytes remains a leading therapeutic approach for cardiac regeneration after myocardial infarction.
Does siRNA-mediated silencing of Rb1 and Meis2 promote adult cardiomyocyte proliferation and improve cardiac function post-myocardial infarction?
Population
Isolated adult rat cardiomyocytes, human iPSC-derived cardiomyocytes, and in vivo myocardial infarction model
Comparison
siRNA-mediated knockdown of Rb1 and Meis2
Design
Preclinical in vitro and in vivo study
Authors
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May promote post-MI repair in animals; leaves open clinical translation pending human trials.
Does siRNA-mediated silencing of Rb1 and Meis2 promote adult cardiomyocyte proliferation and improve cardiac function post-myocardial infarction?
Silencing senescence-associated genes Rb1 and Meis2 in adult cardiomyocytes promotes cell cycle reentry, reduces infarct size, and improves cardiac function post-myocardial infarction in preclinical models.
Alam et al. (2019) studied Myocardial infarction. Small interfering RNA-mediated silencing of Rb1 and Meis2 was evaluated on Cardiomyocyte proliferation, infarct size, and cardiac function. Silencing of Rb1 and Meis2 in adult cardiomyocytes resulted in marked cardiomyocyte proliferation, reduced infarct size, and improved cardiac function post-myocardial infarction.
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