ArticleBMC microbiology2025
Mouse models of aortic dissection induced by β-aminopropionitrile combined with angiotensin II and the changes in their gut microbiota.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- DTX1 Regulates Aortic Dissection Progression by Modulating Vascular Smooth Muscle Cell Phenotypic Switching via Ubiquitination of ITGA5.Cardiovascular drugs and therapy · 2026Article
- Animal Models of Aortic Aneurysm and Dissection: A Comparative Guide for Mechanism, Therapeutic Testing, and Translational Readouts.Biomedicines · 2026Review
- Study on the mechanism of action of Kangfuxin liquid in alleviating DSS-induced ulcerative colitis in mice.Frontiers in pharmacology · 2026Article
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8 authors.
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Abstract
backgroundAortic dissection (AD) is a lethal vascular disease with no effective pharmacological treatments currently available. The construction of mouse models is crucial for researching the pathogenesis of AD. The gut microbiota play a role in the progression of AD, but studies on their changes in AD mouse models are lacking. This study compares various strategies for constructing mouse models of acute AD and examines changes in their gut microbiota.
resultsAcute AD models were created using male C57BL/6J mice aged 5-6 weeks, induced with β-aminopropionitrile (BAPN) combined with angiotensin II (Ang-II). The models differed in terms of dosage, timing, and path of administration. The treatment groups were compared in terms of general condition, blood glucose level, blood pressure, and rate of dissection formation and mortality. Hematological and histological changes of the tissues were analyzed. Changes in gut microbiota were determined through 16 S rDNA sequencing. All five strategies successfully induced AD in mice. BAPN at 1 g/kg/day combined with subcutaneous injection of Ang-II induced acute AD with higher incidence rates and lower mortality rate within 2 weeks. Regardless of the construction strategy, the AD mice showed similar changes in gut microbiota, displaying increased alpha and beta diversity. The relative abundance of Actinobacteria and Bacteroidetes increased and that of Firmicutes and Proteobacteria decreased. Ligilactobacillus, Escherichia, Enterobacteriaceae, and Gammaproteobacteria were dominant in the control group, whereas Muribaculaceae, Lactobacillus, Duncaniella, COE1, and Limosilactobacillus were dominant in the AD model group. Ligilactobacillus was significantly negatively correlated with the maximum diameters of the thoracic and abdominal aortas, whereas CAG-485 showed a significant positive correlation.
conclusionsBAPN at 1 g/kg/day combined with subcutaneous injection of Ang-II is a stable and efficient method to induce acute AD in mice. Dysbiosis occurred in all groups, with a high degree of consistency across construction strategies.
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