ReviewAnimal models and experimental medicine2025
Animal models for abdominal aortic aneurysms: Where we are and where we need to go.
Review in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Nicotinamide adenine dinucleotide phosphate hydrogen oxidase 2 exacerbates abdominal aortic aneurysm formation by inducing oxidative stress through autophagy inhibition.Histology and histopathology · 2026Article
- Inhibition of STING pathway attenuates experimental abdominal aortic aneurysm progression.Acta pharmacologica Sinica · 2026Article
- Integrin Signaling Pathways in Aortic Aneurysm and Dissection.Reviews in cardiovascular medicine · 2026Review
- Cytokine-Family Biomarker Candidates for Small Abdominal Aortic Aneurysm Identified via Integrated mRNA and Protein Expression Profiling.International journal of molecular sciences · 2026Article
- Cytoskeletal-related genes function as checkpoints for the maintenance of VSMC contractile phenotype and prevent pathological remodeling in arterial diseases.Journal of advanced research · 2026Article
- An endovascular porcine model of abdominal aortic aneurysm for interventional radiology research.European radiology experimental · 2026Article
- Perivascular adipose tissue inflammation in abdominal aortic aneurysm: An underrecognized contributor.Journal of biomedical research · 2025Article
- Multifunctional nanoparticles in abdominal aortic aneurysm management: from basic research to clinical transformation.Journal of nanobiotechnology · 2025Review
- Animal models for abdominal aortic aneurysms: Where we are and where we need to go.Animal models and experimental medicine · 2025Review
Corrections and comments
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Authors and funding
3 authors.
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Abstract
The mortality rate of patients with abdominal aortic aneurysm (AAA) after rupture is extremely high, and this disease has become an important disease endangering the health of the Chinese population. Methods used to model AAA include intraluminal pressurized elastase infusion, chronic infusion of angiotensin II (Ang II) via an osmotic pump, periarterial application of calcium chloride, vascular grafting, and gene modification. AAA models induced by elastase and Ang II are the two most widely used animal models. In the elastase-induced model, because intraluminal infusion is transient, with the cessation of initial stimulation, the aneurysm lesion tends to be stable and rarely ruptures. The model induced by Ang II infusion often presents with a typical aortic dissection with a false lumen, whereas clinical AAA patients do not necessarily have dissection. Currently, the treatment of AAA in clinical practice remains endovascular, and there is a lack of pharmacological therapy, which is also related to the fact that the pathogenic mechanism has not been fully elucidated. Smoking, old age, male sex, and hypertension are the main risk factors for AAA, but these risk factors have not been fully investigated in the current modeling methods, which may affect the clinical translational application of research results based on animal models. Therefore, this article reviews the most commonly used AAA modeling methods, comments on their applications and limitations, and provides a perspective on the development of novel animal models.
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