Human-based electromechanical simulations reveal electrocardiogram biomarkers are better indicators of pro-arrhythmic substrate after myocardial infarction than ejection fraction.
Matthew P Klassen, Christian J Peters ... Yuh Nung Jan
As in humans, Drosophila hearts are able to maintain contractile performance during healthy aging, but this maintenance is associated with an increased susceptibility to progressive dysrhythmias that can lead to fibrillatory arrest.
The HCN1 channel gates thanks to a coupling mechanism involving the reorganization of the interfaces between the voltage-sensor domains and pore helices, subtly shifting the balance between hydrophobic and hydrophilic interactions in a 'domino effect'.
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.
Giovanni Stefano Ugolini, Andrea Pavesi ... Monica Soncini
Human cardiac fibroblasts regulate their cellular responses according to the combination of multiple environmental stimuli namely oxygen changes and mechanical signals.
Hirohito Shimizu, Johann Schredelseker ... Jau-Nian Chen
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.
Mario García-Navarrete, Merisa Avdovic ... Krzysztof Wabnik
A combination of mathematical modeling and live-cell imaging reveals a strategy for the rational control over cell electrophysiology though modulation of ion channel expression.
ML277 exclusively enhances the AO state voltage-sensing domain (VSD)-pore coupling of KCNQ1 channels, providing an effective tool to investigate the voltge-dependent gating and new strategies for treating long QT syndrome.
Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.
