Vinay R. Penna

This study shows that blocking CD14 reduces arrhythmogenic cardiomyopathy in mice by decreasing inflammation and fibrosis.

Human arrhythmogenic cardiomyopathy hearts harbor a lesion niche of POSTN fibroblasts and NLRP3+ inflammatory macrophages; IL-1β neutralization in Dsg2-mutant mice reduced fibrosis, dysfunction, and ventricular ectopy.

This study shows that inhibiting soluble epoxide hydrolase reduces inflammation and myocardial injury in arrhythmogenic cardiomyopathy by increasing pro-resolving lipid mediators.