Firre promotes myocardial proliferation and repair via binding to PTBP1 and activating the Akt pathway

After birth, the newborn mammalian heart retains a temporary regenera-tive capacity that eventually fades with age. Resuming the proliferation of cardiomyocytes is becoming a crucial tactic in promoting heart repair. The current study found that the newborn heart had an overexpression of the long-stranded noncoding RNA element (FIRRE), which is positioned in the nucleus and plays a crucial function in cardiac development and repair. In vitro tests demonstrated that cardiomyocytes with overexpressed LncFirre experienced enhanced cell entrance into the S phase and boosted cell pro-liferation. In vivo, cardio-myocyte proliferation was enhanced, scar size was decreased, and the regeneration window of the neonatal mouse myocardi-um was extended by the delivery of AAV9-LncFirre. LncFirre enhanced heart function, decreased infarct size, and encouraged cardiomyocyte proliferation in adult mice suffering from myocardial infarction.