Does deletion of EP4 on bone marrow-derived cells enhance inflammation and angiotensin II-induced abdominal aortic aneurysm formation?
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.
There was no added predictive value of MetS beyond its individual components with respect to mortality risk. Attention should be redirected to the individual components, particularly visceral obesity and high glucose, to treat each abnormality appropriately.