Project description:There is no effective pharmacotherapy to prevent the growth and rupture of abdominal aortic aneurysms (AAA), a leading cause of death. We developed a novel preclinical model showing that the interaction of bona fide risk factors (i.e., cigarette smoke (CS) and hypercholesterolemia) induced AAA formation, rupture, and death. Elastin fragmentation resulted from CS-induced exacerbation of the atherosclerotic process, significant given atherosclerosis is a disease of the inner intimal layer of the artery, with the media remaining largely intact. Importantly, arterial injury was driven by CSF-1-dependent macrophages (Mφ) accumulating within developing atherosclerotic plaques that exhibited tissue degrading proteolytic activity in vivo. Single-cell RNA sequencing further demonstrated conservation of Mφ responses in atherosclerotic plaque from murine and human AAA. Our findings advance understanding of the pathological sequelae of atherosclerosis, establishing plaque Mφ as important mediators of tissue damage and a potential target for prevention of AAA growth and rupture.

2025-03-06 | GSE284253 | GEO

Cytokines in Abdominal Aortic Aneurysm: Master Regulators With Clinical Application.

Project description: Not available

| S-EPMC9052234 | biostudies-literature

Recombinant Decorin Fusion Protein Attenuates Murine Abdominal Aortic Aneurysm Formation and Rupture.

Project description: Not available

| S-EPMC5696466 | biostudies-literature

Phosphorylation of AKT and abdominal aortic aneurysm formation.

Project description: Not available

| S-EPMC3873487 | biostudies-literature

CTRP13 Mitigates Abdominal Aortic Aneurysm Formation via NAMPT1.

Project description: Not available