Preprint provides in vivo genetic evidence that cardiomyocytes can undergo mesenchymal-like transition in myocardial fibrosis

A preprint deposited on bioRxiv presents evidence that cardiomyocytes — the contractile cells of the heart — can undergo a mesenchymal-like fate transition during myocardial fibrosis, challenging the long-standing view that cardiac fibrosis results exclusively from the activation of resident fibroblasts.

The study combined immunohistochemical analysis of human myocardial infarction tissue with in vivo genetic lineage-tracing experiments in mouse models to track the fate of cardiomyocytes during pathological remodelling. The authors report that a proportion of cardiomyocytes acquire mesenchymal characteristics, and begin to elucidate the regulatory mechanisms underlying this transition. Myocardial fibrosis is a hallmark of adverse cardiac remodelling and a major contributor to heart failure progression.

The findings, if confirmed by peer review and independent replication, could have implications for how researchers conceptualise the cellular origins of cardiac fibrosis, with potential longer-term relevance for therapeutic strategies targeting fibrotic pathways. As a preprint, this work has not yet been independently peer-reviewed and should be treated as preliminary.