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.

Modest changes in expression of interacting dose-dependent transcription factors Tbx5 and Prrx1, caused by disease-associated common regulatory variants, significantly impact on the cardiac gene regulatory network and disease susceptibility.

In models reconstructed from MRI scans of patients with embolic stroke of undetermined source, computational simulations reveal that fibrosis has the intrinsic capacity to sustain arrhythmia drivers when subjected to triggered activity known to exist in patients with atrial fibrillation.

Excitability gradients in heart tissue, imposed by structured sub-threshold optogenetic stimulation, induce drift and termination of spiral waves, thus providing an explanation for successful optogenetic defibrillation in small animal hearts.

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.

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.

Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.

Aβ inhibitors effectively block its aggregation, while also reducing seeding of tau aggregation from Aβ, tau, and AD derived fibrils, suggesting the two share a structurally related disease relevant interface.

Integrative structural biology reveals a conformational equilibrium in the Box C/D methylation enzyme that regulates the extent of site-specific 2'-O-rRNA methylation in dependence of the RNA sequence.

Vigorous endurance training results in prolongation of cardiac repolarization and increased repolarization instability, mild ventricular fibrosis associated with decrease of the transient outward potassium current, and enhanced arrhythmia susceptibility in canine model.