Cardiac conduction system regeneration prevents arrhythmias after myocardial infarction.

Arrhythmias are a hallmark of myocardial infarction (MI) and increase patient mortality. How insult to the cardiac conduction system causes arrhythmias following MI is poorly understood. Here, we demonstrate conduction system restoration during neonatal mouse heart regeneration versus pathological remodeling at non-regenerative stages.

Rapid neutrophil mobilization by VCAM-1+ endothelial cell-derived extracellular vesicles.

Aims: Acute myocardial infarction rapidly increases blood neutrophils (<2 h). Release from bone marrow, in response to chemokine elevation, has been considered their source, but chemokine levels peak up to 24 h after injury, and after neutrophil elevation. This suggests that additional non-chemokine-dependent processes may be involved.

A Refined Protocol for Coronary Artery Ligation in the Neonatal Mouse.

The neonatal mouse heart can regenerate following myocardial infarction (MI), a capacity that is lost after 7 days, providing a model system to study tissue regeneration and the transition to adult wound healing. MI can be induced in neonatal mice surgically by coronary artery ligation. In this protocol, neonates are anesthetized using a combination of inhaled isoflurane anesthesia and induced hypothermia, a significant ethical refinement over previous protocols.

Mouse models of myocardial infarction: comparing permanent ligation and ischaemia-reperfusion.

Myocardial infarction (MI) is a disease of major consequence in the modern world, causing permanent, irreversible damage to the heart. Survivors are at risk for developing further cardiovascular pathologies such as heart failure. Further study of MI injury is crucial to improve the understanding and treatment of the post-MI heart.