This cascade led to a metabolic transition into glycolysis in cardiac macrophages and the secretion of IL-1β, which contributed to intramyocardial inflammation, adverse ventricular remodeling, and impaired contractile function.301 LGR4 is a member of the leucine-rich repeat-containing G protein-coupled receptor (LGR) family and is highly expressed on the membranes of cardiac macrophages after myocardial infarction. Here, IL1B is linked to myocardial infarction.