Human cardiomyopathy mutations induce myocyte hyperplasia and activate hypertrophic pathways during cardiogenesis in zebrafish.
Hadp1, a newly identified pleckstrin homology domain protein, is required for cardiac contractility in zebrafish.
The regenerative capacity of zebrafish reverses cardiac failure caused by genetic cardiomyocyte depletion.
The zebrafish as a novel animal model to study the molecular mechanisms of mechano-electrical feedback in the heart.
Fine mapping of the 1p36 deletion syndrome identifies mutation of PRDM16 as a cause of cardiomyopathy.
