Cardiovascular disease is a health hazard to humans and systolic heart failure due to myocardial infarction is a major cause of death. It was previously thought that myocardial cells of adult mammalian heart possess a limited ability to proliferate and renew themselves, and that after ischemic injury, a large number of myocardial cells are lost and eventually replaced by non-contractile scar tissue. In contrast, it has been widely reported that mammals have the ability to regenerate myocardium which is restricted to early postnatal life, and that it is strong enough to repair damaged heart tissue. The discovery of myocardial regeneration in neonatal heart has provided an ideal animal model to investigate the mechanisms that affect myocardial cell proliferation, and subsequently many mechanisms that can reverse myocardial cell cycle arrest and promote myocardial cell proliferation have been revealed. In this paper, we review the factors affecting myocardial regeneration gene expression (ncRNAs, transcription factors, etc.), myocardial regeneration-related signaling pathways, and the regulation of myocardial regeneration by non-myocardial cells (extracellular matrix, immune response, epicardium, etc.), so as to provide directions for achieving myocardial regeneration after myocardial injury in adult mammals.