Animal Models of Aortic Aneurysm and Dissection: A Comparative Guide for Mechanism, Therapeutic Testing, and Translational Readouts

Aortic aneurysms and dissections are devastating vascular diseases with high mortality, yet no pharmacological therapy has proven effective in halting growth or preventing rupture. Surgical and endovascular repair remain the only treatment options for advanced disease. Animal models have been indispensable in defining mechanisms and testing candidate therapies, but the diversity of protocols, strain-dependent variability, and heterogeneous endpoints complicate interpretation and translation. This review provides an update focused on how to match models to specific research questions. We critically compare commonly used abdominal aortic aneurysm (AAA) models (angiotensin II ± hyperlipidemia, elastase, calcium chloride, β-aminopropionitrile BAPN hybrids, and mineralocorticoid agonist/fludrocortisone models) with thoracic aortopathy and dissection models (BAPN alone or with AngII, genetic models including Marfan and smooth muscle contractile mutations, and AngII + TGF-β blockade). We highlight practical considerations on segment specificity, rupture incidence, lipid dependence, comorbidities, and outcome measurement, with emphasis on rigor and reporting standards. A translational thread on platelet-intraluminal thrombus biology, including the emerging biomarker and therapeutic targets such as glycoprotein VI (GPVI), is integrated across models. We offer a decision grid and rigor checklist to harmonize model use, enhance reproducibility, and accelerate translation.