Related Experiment Video
Updated: Oct 11, 2025
05:31
Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
Published on: May 16, 2025
379
Neuraminidase 1 Exacerbating Aortic Dissection by Governing a Pro-Inflammatory Program in Macrophages
Qian Wang1, Zhaoyang Chen2, Xiaoping Peng3,4
1Department of Blood Transfusion, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Frontiers in Cardiovascular Medicine
|December 6, 2021
Summary
Macrophage-derived neuraminidase 1 (NEU1) is crucial for aortic homeostasis. Inhibiting NEU1 improves aortic function and reduces rupture risk in a mouse model of aortic dissection, suggesting NEU1 as a therapeutic target.
Area of Science:
- Vascular Biology
- Immunology
- Enzymology
Background:
- Inflammation and macrophages are key in aortic dissection (AD).
- Neuraminidases (NEUs) regulate macrophage immune responses.
- The role of neuraminidase 1 (NEU1) in AD pathogenesis is unclear.
Purpose of the Study:
- To investigate the role of NEU1 in pathological aortic degeneration.
- To elucidate the mechanism of NEU1 in aortic dissection.
Main Methods:
- Used a mouse model of aortic dissection induced by β-aminopropionitrile monofumarate (BAPN).
- Generated global and macrophage-specific NEU1 knockout (NEU1 CKO) mice.
- Analyzed aortic function, inflammation, apoptosis, oxidative stress, extracellular matrix degradation, and macrophage polarization.
Main Results:
- NEU1 expression increased in aortic lesions after BAPN administration.
- NEU1 CKO mice showed improved aortic function, reduced mortality, and attenuated vascular inflammation.
- NEU1 deficiency mitigated apoptosis, reactive oxygen species, extracellular matrix degradation, and promoted M2 macrophage polarization.
Conclusions:
- Macrophage-derived NEU1 is essential for vascular homeostasis.
- NEU1 exacerbates BAPN-induced pathological aortic remodeling.
- NEU1 represents a potential therapeutic target for aortic dissection.
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