In the mouse ischaemic myocardium, neutrophils promote ventricular tachycardia via the secretion of resistin-like molecule-γ (RELMγ), a pore-forming peptide that damages the membranes of cardiomyocytes. This finding, published in Science, highlights RELMγ as a potential therapeutic target to prevent arrhythmia after myocardial infarction (MI).

“We have learned recently that MI triggers a huge influx of immune cells, including neutrophils, into the myocardium, but until now, whether and how these cells contribute to cardiac arrhythmias that are particularly common in patients with acute MI was not clear,” explains Matthias Nahrendorf, the senior author of the study.