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

Targeting mir128-3p could prevent cardiac insulin resistance in the non-infarcted myocardium and limit cardiac injury after myocardial infarction, delaying the development of heart failure.

Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.

4,6-Sulfation of chondroitin sulfate proteoglycans prevents sympathetic nerve regeneration into the infarct after myocardial ischemia/reperfusion, and reducing this sulfation promotes nerve regeneration and decreases arrhythmia susceptibility.

Immature CD10^neg neutrophils and CD14⁺HLA-DR^neg/low monocytes inducing proinflammatory and adaptive immune responses emerge in patients with large acute myocardial infarction.

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.

Pharmacological and genetic blockade of β1-AR-Gαs signaling prolongs the cardiac regenerative window in juvenile mouse by activating YAP.

SARS-CoV-2 infection in hamsters causes cardiovascular pathologies.

The transcriptional landscape of epicardial cells revealed 11 cell populations that differentially expressed early cardiac genes and numerous cardioprotective paracrine factors defining their regenerative potential.