Regenerative Capacity of Heart Tissue Explored

University of Texas Southwestern Medical Center (Texas, USA) researchers have pinpointed a molecular mechanism needed to unleash the heart's ability to regenerate, a critical step toward developing eventual therapies for damage suffered following a heart attack.  In a mouse model, Hesham Sadek and colleagues found that microRNAs – tiny strands that regulate gene expression – contribute to the heart's ability to regenerate.   The hearts of young rodents mounted a robust regenerative response following myocardial infarction, but this restorative activity only occurs during the first week of life. The team  then discovered that a microRNA called miR-15 disables the regenerative capacity after one week, but when miR-15 is blocked, the regenerative process can be sustained much longer.  By determining the fundamental mechanisms that control the heart's natural regenerative on-off switch, researchers have begun to better understand the No. 1 hurdle in cardiovascular research – the inability of the heart to regenerate following injury.  The study authors conclude that: “the neonatal mammalian heart can regenerate after myocardial infarction through proliferation of preexisting cardiomyocytes and that the miR-15 family contributes to postnatal loss of cardiac regenerative capacity.”