ArticleArteriosclerosis, thrombosis, and vascular biology2022
Adipocyte-Derived Serum Amyloid A Promotes Angiotensin II-Induced Abdominal Aortic Aneurysms in Obese C57BL/6J Mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Role of adipocyte angiotensinogen or angiotensin type 1a receptors in the development of diet-induced atherosclerosis or angiotensin II-induced abdominal aortic aneurysms.JVS-vascular science · 2026Article
- Perivascular adipose tissue inflammation in abdominal aortic aneurysm: An underrecognized contributor.Journal of biomedical research · 2025Article
- Serum Amyloid A: A Double-Edged Sword in Health and Disease.International journal of molecular sciences · 2025Review
- Age-related obesity and inflammaging in cats.Frontiers in veterinary science · 2025Review
- Macrophage ILF3 promotes abdominal aortic aneurysm by inducing inflammatory imbalance in male mice.Nature communications · 2024Article
- Antisense oligonucleotide targeting hepatic Serum Amyloid A limits the progression of angiotensin II-induced abdominal aortic aneurysm formation.Atherosclerosis · 2024Article
- A preliminary study of sirtuin-1 on angiotensin II-induced senescence and inflammation in abdominal aortic aneurysms.CytoJournal · 2024Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundObesity increases the risk for human abdominal aortic aneurysms (AAAs) and enhances Ang II (angiotensin II)-induced AAA formation in C57BL/6J mice. Obesity is also associated with increases in perivascular fat that expresses proinflammatory markers including SAA (serum amyloid A). We previously reported that deficiency of SAA significantly reduces Ang II-induced inflammation and AAA in hyperlipidemic apoE-deficient mice. In this study. we investigated whether adipose tissue-derived SAA plays a role in Ang II-induced AAA in obese C57BL/6J mice.
methodsThe development of AAA was compared between male C57BL/6J mice (wild type), C57BL/6J mice lacking SAA1.1, SAA2.1, and SAA3 (TKO); and TKO mice harboring a doxycycline-inducible, adipocyte-specific SAA1.1 transgene (TKO-Tg
resultsIn response to Ang II infusion, SAA expression was significantly increased in perivascular fat of obese C57BL/6J mice. Maximal luminal diameters of the abdominal aorta were determined by ultrasound before and after Ang II infusion, which indicated a significant increase in aortic luminal diameters in wild type and TKO-TG
conclusionsWe demonstrate for the first time that SAA deficiency protects obese C57BL/6J mice from Ang II-induced AAA. SAA expression only in adipocytes is sufficient to cause AAA in obese mice infused with Ang II.
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