Experimental Models of Abdominal Aortic Aneurysms

Tsui, Janice

doi:10.2174/1874192401004010221

Cited by 37 publications

(32 citation statements)

References 99 publications

(105 reference statements)

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“…In addition, there is a xenograft rat model of AAA, which results in aortic dilatation and the presence of a mural thrombus in ~20% of rats (17). However, AngII infusion is the only consistent mouse model of aortic dilatation and rupture (3, 4, 18). …”

Section: Introductionmentioning

confidence: 99%

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Owens

Edwards

Antoniak

et al. 2015

ATVB

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Objective Rupture of abdominal aortic aneurysms (AAAs) causes a high morbidity and mortality in the elderly population. Platelet-rich thrombi form on the surface of aneurysms and may contribute to disease progression. In this study, we used a pharmacologic approach to examine a role of platelets in established aneurysms induced by angiotensin II (AngII) infusion into hypercholesterolemic mice. Approach and Results Administration of the platelet inhibitors aspirin (ASA) or clopidogrel bisulfate to established AAAs dramatically reduced rupture. The mechanism of protection appears to be a reduction in abdominal aortic platelet and macrophage recruitment resulting in decreased active matrix metalloproteinases (MMPs) 2 and 9. Platelet inhibitors also resulted in reduced plasma concentrations of platelet factor 4, cytokines, and components of plasminogen activation system in mice. To determine the validity of these findings in human subjects, eligible aneurysm patients were retrospectively analyzed using developed and validated algorithms in the electronic medical record database at Vanderbilt University. Similar to mice, administration of ASA or P2Y12 inhibitors was associated with reduced death amongst AAA patients. Conclusions These results suggest that platelets contribute to AAA progression and rupture.

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Section: Introductionmentioning

confidence: 99%

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Owens

Edwards

Antoniak

et al. 2015

ATVB

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“…27 Surgery is the only effective treatment, and the mortality associated with AAA is still ≈50%. 28 Moreover, there are no specific pharmacological therapies to prevent the progression of small AAAs. 4 Thus, it is necessary to develop a new, effective strategy of drug treatment.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting the Th17/IL-17A–Related Inflammatory Responses With Digoxin Confers Protection Against Experimental Abdominal Aortic Aneurysm

Wei

Wang

Zhang

et al. 2014

ATVB

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A bdominal aortic aneurysm (AAA) is a common disease affecting elderly males, with an incidence of 1.3% in men 45 to 54 years old and 12.5% in men 75 to 84 years old, especially in Western countries.1 Aortic rupture carries a 75% to 90% mortality rate, which is related to aortic diameter.2 Surgical repair is the only efficient treatment for elective patients with large AAAs (aorta diameter ≥5.5 cm). However, based on aneurysm screening programs in the United States, >90% (≈360 000) of aneurysms were small aneurysms (3.0 cm

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“…Both the apoE À/À and the LDLR À/À mice develop aneurysms and atherosclerotic lesions throughout the length of the aorta if fed high cholesterol diets [82,83]. Although the apoE-deficient mouse has limited applicability to humans, both the apoE-deficient mice and the LDLR-deficient mice highlight the role of lipid metabolism in the development of AAA [84]. Other mice targeting specific cardiovascular pathways related to AAA have also been developed.…”

Section: Genetic Modelsmentioning

confidence: 99%

“…Tsukuba hypertensive mice were created by targeting the RAS and crossing mice expressing human renin or human angiotensinogen [79]. The resulting offspring of the transgenic mice died of ruptured aneurysms when fed water with 1% sodium chloride [84]. Genes related to ECM degradation have also been targets for mouse model development.…”

Section: Genetic Modelsmentioning

confidence: 99%

“…Sweet pea meal Copper metabolism No [74] X-chromosome abnormality X chromosome abnormality Copper metabolism No [76] Lysyl oxidase (Lox) Lysyl oxidase deficient mouse Extracellular matrix No [108] Apolipoprotein E (ApoE) ApoE deficient mouse RAS No [81,82] Low-density lipoprotein receptor (LDLR) LDLR deficient mouse Lipid metabolism Yes [82,84] Transgenic renin and angiotensin Transgenic mice expressing human renin and angiotensin RAS Yes [79] Matrix metallopeptidase (MMP-3) MMP3 deficient mouse Extracellular matrix degradation Yes [85] Tissue inhibitor of matrix metallopeptidase (TIMP-1)…”

Section: Broad Breasted Bronze and American Mammoth Bronze Turkeymentioning

confidence: 99%

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An update on the etiology of abdominal aortic aneurysms: implications for future diagnostic testing

Miner

Faries

Costa

et al. 2015

Expert Review of Cardiovascular Therapy

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Abdominal aortic aneurysm (AAA) disease is multifactorial with both environmental and genetic risk factors. The current research in AAA revolves around genetic profiles and expression studies in both human and animal models. Variants in genes involved in extracellular matrix degradation, inflammation, the renin-angiotensin system, cell growth and proliferation and lipid metabolism have been associated with AAA using a variety of study designs. However, the results have been inconsistent and without a standard animal model for validation. Thus, despite the growing body of knowledge, the specific variants responsible for AAA development, progression and rupture have yet to be determined. This review explores some of the more significant genetic studies to provide an overview of past studies that have influenced the current understanding of AAA etiology. Expanding our understanding of disease pathogenesis will inform research into novel diagnostics and therapeutics and ultimately to improve outcomes for patients with AAA.

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Experimental Models of Abdominal Aortic Aneurysms

Cited by 37 publications

References 99 publications

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Platelet Inhibitors Reduce Rupture in a Mouse Model of Established Abdominal Aortic Aneurysm

Inhibiting the Th17/IL-17A–Related Inflammatory Responses With Digoxin Confers Protection Against Experimental Abdominal Aortic Aneurysm

An update on the etiology of abdominal aortic aneurysms: implications for future diagnostic testing

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