β-adrenergic receptors at the Golgi apparatus activate a local signaling pathway, not accessed by cell surface receptors, to drive cardiac hypertrophy and could represent a target for heart failure therapy.
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.
Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.
Transient Ca elevations of cytoplasmic calcium in cardiac myocytes profoundly activate cardiac Na/K pump activity in parallel with physical-chemical changes of the sarcolemma but without involvement of conventional signaling mechanisms.
The ion channel accessory subunit KChIP2 has a transcriptional role that provides regulation over miRNA targets, driving the adverse remodeling of key ion channels during cardiac stress and leading to the development of arrhythmia.