Abstract
Mammalian heart is considered postmitotic with limited cardiomyocyte (CM) turnover during lifetime of an individual [1]. Adult CMs are typically unable to complete the cell cycle and respond to growth signals by hypertrophy or incomplete cytokinesis resulting in binucleation and/or polyploidization, considered to be major hurdles in CM proliferation and regeneration [2]. Ensuing years have seen a tremendous effort to delineate CM cell cycle and develop strategies that promote cell cycle reentry and CM mediated regeneration of the heart following injury.
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