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Semaglutide Prevents Aortic Rupture and Dissection in the Angiotensin II Mouse Model
Amanda Balboa Ramilo1, Kevin Mani2, Anders Wanhainen2
1Department of Medical Cell Biology, Uppsala University, 751 23 Uppsala, Sweden.
Biomedicines
|May 4, 2026
Summary
Semaglutide, a Glucagon-like peptide-1 receptor agonist (GLP-1RA), prevents early aortic rupture and dissection in a mouse model of abdominal aortic aneurysm (AAA). It may preserve vessel wall integrity by maintaining collagen content.
Area of Science:
- Vascular Biology
- Pharmacology
- Medical Research
Background:
- Abdominal aortic aneurysm (AAA) is a dangerous vascular disease with no current pharmacological prevention.
- Glucagon-like peptide-1 receptor agonists (GLP-1RAs) show potential in reducing AAA-related risks.
- Semaglutide, a potent GLP-1RA, warrants investigation for AAA prevention.
Purpose of the Study:
- To investigate the preventative effects of semaglutide on AAA development and rupture.
- To explore the underlying mechanisms of semaglutide's action in a murine AAA model.
Main Methods:
- AAA was induced in apolipoprotein-E-deficient mice using angiotensin II infusion.
- Mice received semaglutide either prophylactically or as a rescue treatment.
- Aortic diameter was measured via ultrasound, and aortic tissue underwent histological analysis.
Main Results:
- Prophylactic semaglutide significantly reduced early mortality from rupture and dissection.
- AAA formation at 28 days was not affected by semaglutide treatment.
- Histology at day seven indicated preserved vessel wall thickness and a trend towards increased collagen content with semaglutide.
Conclusions:
- Semaglutide demonstrates efficacy in preventing early aortic rupture and dissection in an angiotensin II-induced AAA mouse model.
- The protective effect may be attributed to semaglutide's role in maintaining collagen proportion in the early stages of AAA development.
