Revealing Pathways of Cardiac Regeneration
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
See Article by Adamowicz, Morgan, and Haubner et al
Major cardiac injuries like a large myocardial infarction lead to systolic heart failure because of loss of cardiomyocytes. Unlike during embryonic development,1 adult mammalian cardiomyocytes have limited ability to proliferate and replenish the adult mammalian heart. Although there was once excitement over possible adult cardiac stem cells residing in the mammalian myocardium, it now seems that there are insufficient cardiac progenitor cells in the heart2 to generate any meaningful regeneration. More recently, it was discovered that the heart’s regenerative ability is preserved in the first hours after birth in mice3 and rats.4 Indeed, cardiac regeneration may be recapitulated in vitro using immature human heart organoids,5 indicating an innate capacity of some cardiomyocytes for regeneration. These and other recent discoveries have advanced our understanding of how the mammalian heart can regenerate under certain circumstances, potentially setting the stage for us to appreciate why adult human hearts fail to regenerate.
Modern genomic technology can provide a broad molecular characterization of specific cell and tissue states. In this issue of Circulation: Genomic and Precision Medicine, Adamowicz et al6 present a wealth of data regarding the total transcriptomic profile of newborn mouse hearts under normal (physiological) development and during the regenerative response after myocardial infarction. Here, using RNASeq technology, they reveal not only the relative amount of messenger RNAs but also lncRNAs and microRNAs in a time-course study. Left ventricular samples were collected within at least 4 time intervals and pairwise compared between the conditions (Figure).