Single-cell RNA sequencing reveals Nrg1/ErbB2-induced metabolic reprogramming as a pivotal event for cardiomyocyte proliferation during heart regeneration.

The transcription factor Nr2f1a represses ventricular and pacemaker cardiomyocyte identities within distinct regions of the zebrafish atrium.

Compliant matrix provides a permissive micoenvironment for cardiomyocyte dedifferentiation, cell division and expansion, and thus may open a new avenue towards cardiac regeneration.

The primary respiratory defect seen in aged cardiomyocytes is an elevated proton leak mediated by ANT1, and this is prevented by treatment with SS-31 (elamipretide).

Lineage analysis reveals that cardiac neural crest contributes to cardiomyocytes across vertebrates and consistent with this, the neural crest gene regulatory program is reactivated upon heart regeneration in zebrafish.

Endothelial cells in the heart have transcriptional and epigenetic signatures of cardiomyocytes.

Mammal hearts are unable to replace lost cardiomyocytes, which may be due to the loss of centrosome integrity in these cells after birth.

Single-cell screens during human cardiomyocyte (CM) differentiation reveal that perturbation of congenital heart defect-linked enhancers/genes causes deficient CM differentiation.

Sarcomeres in heart muscle cells come from stress fiber-like structures that are mechanistically distinct from stress fibers in non-muscle cells.

Evolutionarily conserved hypoxic stress response genes are depleted for association with expression quantitative trait loci.