Prostaglandin E2 Receptor 2 Modulates Macrophage Activity for Cardiac Repair

The study demonstrated that the prostaglandin E2 receptor 2 (EP2) played a crucial role in cardiac repair by modulating macrophage activity. Using EP2-deficient transgenic mice, researchers found that the absence of EP2 impaired macrophage recruitment to injured myocardium, leading to reduced tissue repair and worse cardiac performance post-injury. EP2 deficiency altered the proinflammatory response and increased the expression of erythroid differentiation regulator 1 (Erdr1) in macrophages, impairing their migration ability. Knocking down Erdr1 restored macrophage migration. The findings suggested that EP2 signaling was critical for regulating macrophage mobilization and cardiomyocyte regeneration, indicating that EP2 agonists could potentially serve as immune modulators to regulate early inflammatory responses after myocardial infarction.