Deletion of EP4 on Bone Marrow–Derived Cells Enhances Inflammation and Angiotensin II–Induced Abdominal Aortic Aneurysm Formation

Abstract

Deficiency of EP4 on bone marrow-derived cells boosted inflammation and AAA formation induced by angiotensin II in hyperlipidemic mice. This study affirms the pathophysiologic importance of PGE(2) signaling through EP4 as an endogenous anti-inflammatory pathway involved in experimental aneurysm formation.