Cardiomyocyte proliferation and dedifferentiation mediated by OSM in heart regeneration

Background Neonatal mouse heart can completely regenerate after amputating 15%of ventricular apex.However,the regenerative ability is lost by 7 day-post-birth.Cardiomyocyte dedifferentiation is the only way of existing myocytes returning to cell cycle and initiating proliferation.Oncostatin M(OSM)was demonstrated to promote cardiomyocyte dedifferentiation after cardiac injury,while its role in heart regeneration has not been addressed.Modulating the progress of dedifferentiationproliferation through OSM may provide a clinical therapy for preventing further deterioration of patients with heart injury and restoring the lost myocardium.