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.
Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.
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.
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.
Activation of the sarcoplasmic reticulum calcium pump and enhancement of cellular calcium homeostasis by dwarf open reading frame reveal how this small membrane protein opposes phospholamban inhibitory function in cardiac muscle.
Fatty acid analogues are interesting prototype compounds that may inspire the development of future IKs channel activators to treat patients with long QT syndrome caused by diverse arrhythmia-causing mutations in the IKs channel.
The TRPM4 ion channel has been identified as an important component in the causation of mechanical pressure overload-induced pathological left ventricular hypertrophy, which is a powerful predictor of cardiovascular mortality.