TREM1 and triple-A syndrome: In the angiotensin II-induced abdominal aortic aneurysm (AAA) mouse model, AngII enhances TREM-1 production via AngII receptors, which affects monocyte mobilization from the spleen and infiltration into the aortic wall. Consequently, TREM-1 activation promotes monocyte penetration into the aorta and triggers a proinflammatory response, exacerbating AAA severity. Trem1−/− (Apoe−/−Trem1−/−) mice exhibited reduced AAA progression and severity by decreasing aortic inflammation and lowering the expression of Il1b, Tnfa, Mmp2, and Mmp9 mRNA, along with reducing macrophage content.