Enhancing mitochondrial Ca2+ uptake effectively suppresses aberrant Ca2+ induced arrhythmogenic events in zebrafish, mouse and human cardiomyocytes, demonstrating a critical role for mitochondria in the regulation of cardiac rhythmicity.
Transcription-factor-dependent noncoding RNA transcription illuminates components of a transcription-factor-dependent gene regulatory network that includes enhancer-associated long noncoding RNAs and is necessary for cardiac rhythm.
Mapping the locations of hypertrophic cardiomyopathy gene variants onto the three-dimensional structures of contractile proteins revealed that these disrupt protein interactions are critical for normal cardiac relaxation and efficient energy usage.
Loss and gain-of-function investigation uncovers a regulatory network controlling human heart chamber specification in which the cardiac precursor gene ISL1 accelerates ventricular induction and antagonizes retinoic acid-driven atrial commitment.
Cardiac-specific overexpression of a recently discovered micropeptide, DWORF, enhances calcium cycling and contractility in the heart and rescues the heart failure phenotype of a genetic mouse model of dilated cardiomyopathy.
Feedback sensing of the intracellular calcium concentration suffices to reproduce the diversity of ionic conductances underlying normal cardiac electromechanical function in a genetically diverse population of mice.