A computer model of human cardiomyocyte was produced and validated on independent datasets, overcoming shortcomings of its predecessors, also yielding broadly relevant insights and results on major ionic currents.
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.
Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.
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.
TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca2+-dependent pathway for AF risk.
In an empty microglial niche, repopulating microglia arise from subventricular zone and white matter-associated areas without contributions from the bone marrow to fill the mouse brain via a spreading wave.
Brain natriuretic peptide supplementation can increase cardiac neovascularization in infarcted hearts by stimulating endogenous endothelial cell proliferation and proliferation of precursor cells, which will differentiate into endothelial cells.