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The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 ( miR-128 ) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of  miR-128  impairs CM proliferation and cardiac function, while  miR-128  deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses  p27  (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2. Furthermore, deletion of  miR-128  promotes cell cycle re-entry of adult CMs, thereby reducing the levels of fibrosis, and attenuating cardiac dysfunction in response to MI. These results suggest that  miR-128  serves as a critical regulator of endogenous CM proliferation, and might be a novel therapeutic target for heart repair.

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration