Neuregulin1 is induced upon cardiac injury in adult zebrafish, and is sufficient to drive massive proliferative growth of the heart.

Growth-delayed offspring generated from eggs that lacked normal epigenetic programming exhibited a remarkable capacity to undergo late gestational fetal growth recovery, despite inefficient placental function.

Maternal loss of imprinting at the Igf2/H19 locus reduces expression of H19 lncRNA and thereby leads to progressive cardiac pathologies in a mouse Beckwith–Wiedemann syndrome model.

Combined evidence of human genetics, in vitro cardiomyocyte differentiation, and mouse model indicates that SORBS2 is a regulator of second heart field development and its deficiency causes seemingly opposite atrial septal defects.

A novel Mendelian disease featuring early-onset hypertension is caused by a recurrent gain of function mutation in CACNA1H, which encodes the voltage-gated calcium channel Cav3.2.

Discovering that Hoxb1 acts as a repressor of cardiac differentiation on second heart field progenitor cells helps us to understand the etiology of congenital heart defects such as atrioventricular septal defects.

The lncRNA pCharme controls the expression of cardiomyocyte maturation genes and heart development by orchestrating the formation of MATR3-enriched nuclear condensates.

Gene knockout of liver fluke granulin by CRISPR/Cas9 attenuates the virulence of infection with a carcinogenic liver fluke.

Eprhin B1 in the cardiomyocyte regulates the maturation of the adult surface crest architecture and of the diastolic function during a late postnatal stage in rodents.

Ploidy-increasing endocycles may represent a tradeoff between loss of regenerative capacity and preservation of tissue architecture.