Cardiac electrophysiology and arrhythmias

This study shows apremilast improves cardiomyocyte cohesion and reduces arrhythmia in human and murine arrhythmogenic cardiomyopathy models.

The paper develops classifiers to distinguish functional and trafficking effects of KCNQ1 variants, improving variant interpretation for LQTS and channelopathies.

This study modifies a computational model of hiPSC-CMs to compare their excitation properties with hV-CMs under various conditions and finds hiPSC-CMs are more excitable due to their depolarized resting potential and intrinsic automaticity.

This study examines hERG1NP variants linked to sudden death, finding some reduce and others increase hERG1NP activity through different mechanisms.

The paper investigates the role of Na+ and Ca2+ influx in triggering and regulating the calcium transient during the action potential in adult rat cardiomyocytes.

This study identifies a small molecule, VU0494372, that enhances KCNQ1 expression and trafficking, offering a potential therapeutic approach for LQTS.

This study shows that loss of plexin-mediated cardiac innervation leads to adrenergic hypersensitivity and ventricular arrhythmias in mice, with human PLXNA4 variants linked to arrhythmias.

This paper develops and validates sex-specific computational models of human atrial cardiomyocytes to investigate sex differences in atrial fibrillation mechanisms and therapeutic responses.

The paper develops chamber-specific 3D human Engineered Heart Tissue (EHT) models to study KCa2 channel inhibitors and their effects on atrial fibrillation.

This study presents a computational model of the Purkinje network that simulates ischemic effects on conduction and refractoriness, providing insights into arrhythmogenic risk.

This study shows that AaH-II selectively activates TTX-S Nav channels, inducing arrhythmias in cardiac tissue, and suggests targeting these channels as an antiarrhythmic strategy.

This study shows that CaMKII phosphorylation of RYR2 at S2814 is essential for arrhythmia in CPVT, acting as an intra-molecular event.

Arrhythpy quantifies and classifies arrhythmias in iPSC-CMs using Ca2+ transients, showing its utility in disease models and drug response analysis.

This paper shows that obesity-related extracellular vesicles from visceral adipose tissue impair cardiac function and contribute to arrhythmia by affecting cardiomyocytes, fibroblasts, and macrophages.

This study shows that polyamine administration can prolong cardiac repolarization and reduce arrhythmias in a mouse model of SQTS3 caused by Kir2.1M301K mutation.

This study shows that overexpression of Pitx2c in the atria of mice leads to SAN dysfunction and TBS-like pathology, including prolonged SAN recovery time and increased AF inducibility.

The paper uses synthetic data to create digital twins of human cardiomyocytes, enabling precise modeling of electrophysiological properties from experimental recordings.

This study identifies chamber-specific contributions of non-NaV1.5 sodium channel isoforms to cardiac excitability using a chemical-genetic mouse model and electrophysiological recordings.

This study shows that cardiac-specific Kv1.1 deficiency impairs atrial repolarization but does not cause overall cardiac dysfunction or arrhythmia susceptibility.

This study shows dysferlin is critical for maintaining cardiac T-tubule structure and EC coupling, and its loss increases arrhythmia risk under stress and during aging.

This study shows empagliflozin enhances peak sodium current in Nav1.5 channels by acting as a pharmacological chaperone, potentially reducing arrhythmia risk in Duchenne muscular dystrophy.

This study shows that ablating three key phospho-sites in RyR2 preserves adrenergic responses but increases arrhythmogenic risk by altering Ca2+ leak and promoting early afterdepolarizations.

This study shows FGF13 modulates VGSCs by regulating membrane cholesterol, independent of direct channel binding, and reveals its role in maintaining cholesterol distribution and VGSC localization at the intercalated disc.

This paper develops sex-specific human electromechanical models to simulate and evaluate sex differences in drug responses and ECG biomarkers, revealing ionic and anatomical mechanisms underlying these differences.

The paper identifies two strategies using multichannel pharmacology to prolong action potential duration while reducing transmural dispersion of repolarization in cardiac myocytes.

The paper identifies a cardiac neuronal subtype, NA1b, that increases in a murine dilated cardiomyopathy model and shows elevated M-current ion channels and neurodegenerative pathways.

The paper uses patient-derived iPSC-CMs to show that polygenic scores influence cardiac electrophysiology and drug response in Long QT Syndrome.

This study shows that a rare splice mutation in SYNPO2L leads to increased SYNPO2L_B isoform expression, impairing atrial cardiomyocyte function, and that restoring SYNPO2L_A improves electrophysiology and contractility via YAP signaling.