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      TGFβ (Transforming Growth Factor-β) Blockade Induces a Human-Like Disease in a Nondissecting Mouse Model of Abdominal Aortic Aneurysm

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          Abstract

          Current experimental models of abdominal aortic aneurysm (AAA) do not accurately reproduce the major features of human AAA. We hypothesized that blockade of TGFβ (transforming growth factor-β) activity-a guardian of vascular integrity and immune homeostasis-would impair vascular healing in models of nondissecting AAA and would lead to sustained aneurysmal growth until rupture.

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          Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice.

          A Daugherty, M W Manning, L Cassis (2000)
          Increased plasma concentrations of angiotension II (Ang II) have been implicated in atherogenesis. To examine this relationship directly, we infused Ang II or vehicle for 1 month via osmotic minipumps into mature apoE(-/-) mice. These doses of Ang II did not alter arterial blood pressure, body weight, serum cholesterol concentrations, or distribution of lipoprotein cholesterol. However, Ang II infusions promoted an increased severity of aortic atherosclerotic lesions. These Ang II-induced lesions were predominantly lipid-laden macrophages and lymphocytes; moreover, Ang II promoted a marked increase in the number of macrophages present in the adventitial tissue underlying lesions. Unexpectedly, pronounced abdominal aortic aneurysms were present in apoE(-/-) mice infused with Ang II. Sequential sectioning of aneurysmal abdominal aorta revealed two major characteristics: an intact artery that is surrounded by a large remodeled adventitia, and a medial break with pronounced dilation and more modestly remodeled adventitial tissue. Although no atherosclerotic lesions were visible at the medial break point, the presence of hyperlipidemia was required because infusions of Ang II into apoE(+/+) mice failed to generate aneurysms. These results demonstrate that increased plasma concentrations of Ang II have profound and rapid effects on vascular pathology when combined with hyperlipidemia, in the absence of hemodynamic influences.
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            Abdominal aortic aneurysm.

            N Sakalihasan, R Limet, O Defawe (2005)
            Abdominal aortic aneurysms cause 1.3% of all deaths among men aged 65-85 years in developed countries. These aneurysms are typically asymptomatic until the catastrophic event of rupture. Repair of large or symptomatic aneurysms by open surgery or endovascular repair is recommended, whereas repair of small abdominal aortic aneurysms does not provide a significant benefit. Abdominal aortic aneurysm is linked to the degradation of the elastic media of the atheromatous aorta. An inflammatory cell infiltrate, neovascularisation, and production and activation of various proteases and cytokines contribute to the development of this disorder, although the underlying mechanisms are unknown. In this Seminar, we aim to provide an updated review of the pathophysiology, current and new diagnostic procedures, assessment, and treatment of abdominal aortic aneurysm to provide family practitioners with a working knowledge of this disorder.
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              Management of abdominal aortic aneurysms clinical practice guidelines of the European society for vascular surgery.

              F Moll, J T Powell, G Fraedrich … (2011)
              Article 0 comments Cited 227 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Arteriosclerosis, Thrombosis, and Vascular Biology
                Abbreviated Title: Arterioscler Thromb Vasc Biol.
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1079-5642
                ISSN (Electronic): 1524-4636
                Publication date Created: November 2017
                Publication date (Print): November 2017
                Volume: 37
                Issue: 11
                Pages: 2171-2181
                Affiliations
                [1 ]From the Division of Cardiovascular Medicine, University of Cambridge, UK (F.L., M.C., J.R., M.P., L.M., A.F., Z.M.); Université Côte d’Azur, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Institute for Research on Cancer and Aging in Nice, France (F.L., J.R.); University Hospital of Nice, France (F.L, J.R.); Institut National de la Santé et de la Recherche Médicale, Paris Cardiovascular Research Center, France (B.E., M.V., S.T., Z.M.);...
                Article
                DOI: 10.1161/ATVBAHA.117.309999
                SO-VID: 8608095f-3518-45f6-9107-d4ab8cee944c
                Copyright © © 2017
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