Reprogramming cardiomyocytes from other cell types could have therapeutic potential for cardiac diseases. Wang et al. studied the induction of cardiomyocytes from murine fibroblasts. They found that autophagy-related 5 (Atg5) regulated autophagy during early cell reprogramming, whereas the autophagic factor Beclin1 inhibited cardiomyocyte induction.
In cell and mouse models, the authors showed that loss of Beclin1 resulted in gene expression changes in reprogramming cells, activation of Wnt signaling, and reduction of scar size after myocardial infarction. This study helps identify the roles of autophagy-dependent and -independent signaling pathways in cardiac fate determination.