Abstract
Myocardial infarctions (MI) remain a leading cause of global morbidity and mortality, and a reason for this is the inability of adult, mammalian cardiomyocytes to divide post-MI. Recent studies demonstrate a limited population of cardiomyocytes retain their proliferative capacity and understanding how endogenous cardiomyocytes can be stimulated to re-enter the cell cycle is a focus of current research. In this review we discuss the history of zebrafish cardiac regeneration and highlight how different models reveal the molecular pathways important in driving cardiomyocyte proliferation after injury. Understanding the molecules that regulate cell cycle re-entry can provide insights into promoting cardiac repair in humans.