Overview

• Researchers identify Resistin-like molecule gamma (RELMy) from neutrophils as a pore-forming agent that injures cardiomyocyte membranes after myocardial infarction.
• Neutrophil-specific deletion of the Retnlg gene in mouse models cut ventricular tachycardia burden approximately 12-fold.
• Single-cell and spatial RNA sequencing, high-resolution microscopy, liposome assays, and cell culture established the mechanism and functional effects.
• Human infarct tissue showed higher expression of the homolog gene RETN compared with non-infarcted tissue, though functional validation in people is pending.
• The team plans to test neutralization of the protein in animal models to assess whether targeted immune modulation can reduce early post-infarction arrhythmias.