A calcium transient measurement system utilizing human induced pluripotent stem cell-derived cardiomyocytes reveals the detrimental impact of inflammatory cytokines on cardiomyocyte relaxation and displays the potential of drugs to reverse these defects.

Human-based electromechanical simulations reveal electrocardiogram biomarkers are better indicators of pro-arrhythmic substrate after myocardial infarction than ejection fraction.

Eprhin B1 in the cardiomyocyte regulates the maturation of the adult surface crest architecture and of the diastolic function during a late postnatal stage in rodents.

Daily administration of the farnesyltransferase inhibitor lonafarnib decreases central artery stiffness, increases distal artery vasoactivity, and improves left ventricular function consistent with increased survival in a mouse model of Hutchinson-Gilford progeria syndrome.

Activation of TRPV4 induced increases in Ca²⁺ influx, activated CaMKII, enhanced pro-inflammatory NFκB-NLRP3 signaling, and promoted inflammation response, thus contributing to pathological cardiac remodeling.

The transcription factor Meis1 is a dedicated maintenance factor for sympathetic neurons and controls the expression of key genes involved in endosome trafficking.

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.

Inhibition of RyR2 hyperactivity with dantrolene not only prevents VT/VF and SCD but also heart failure by mitigating calcium dysfunction in pressure-overloaded hearts.

Cardiac-specific overexpression of a recently discovered micropeptide, DWORF, enhances calcium cycling and contractility in the heart and rescues the heart failure phenotype of a genetic mouse model of dilated cardiomyopathy.

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.