Overview

• Peer-reviewed findings in Nature Communications identify the prostaglandin E2 receptor EP2 in peripheral Schwann cells as the driver of pain but not inflammation.
• In mice, locally silencing or inhibiting EP2 abolished prostaglandin-mediated pain responses while leaving inflammatory processes intact.
• Experiments in human and mouse Schwann cells showed EP2 activation sustains pain signaling through a pathway separate from inflammation.
• The work shifts focus from earlier emphasis on EP4, presenting EP2 antagonism as a druggable route that may avoid NSAID-related risks.
• Researchers at the NYU Pain Research Center plan further preclinical studies to develop antagonists, assess safety for systemic dosing, and test targeted delivery to joints such as the knee.