1. Academic Validation
  2. Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion

  • J Vis Exp. 2025 May 16:(219). doi: 10.3791/68232.
Yi Zhang 1 Chunyan Wu 2 Chunxiao Wan 3 Naishi Wu 4 Shengkai Zuo 5
Affiliations

Affiliations

  • 1 Department of Cardiovascular Surgery, Tianjin Medical University General Hospital.
  • 2 Department of Biopharmaceutics, Tianjin Key Laboratory of Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University.
  • 3 Department of Physical and Rehabilitation Medicine, Tianjin Medical University General Hospital.
  • 4 Department of Cardiovascular Surgery, Tianjin Medical University General Hospital; wunaishi@tmu.edu.cn.
  • 5 Department of Cardiovascular Surgery, Tianjin Medical University General Hospital; Department of Biopharmaceutics, Tianjin Key Laboratory of Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University; zuoshengkai@tmu.edu.cn.
PMID: 40455668 DOI: 10.3791/68232
Abstract

Thoracic aortic dissection (TAD) is a highly fatal Cardiovascular Disease that lacks efficient medical treatment. Replication of animal models of TAD pathophysiology is essential for studying the intrinsic mechanisms of TAD. The widely used TAD model induced by β-aminopropionitrile (BAPN, an irreversible and orally active Lysyl Oxidase Inhibitor) in mice has the limitation of an inconsistent success rate. This protocol describes in detail a reported modified murine model of TAD induced by oral BAPN combined with subcutaneous angiotensin II (Ang II) infusion. After four weeks of BAPN administration followed by 24 h of Ang II infusion, a murine model with characteristics similar to human TAD was reliably induced, and the success rate of TAD model construction was significantly improved. Oral BAPN inhibits the cross-linking of elastin and Collagen, resulting in the destruction of the aortic wall structure and inducing aortic dilation and dissection formation to a certain extent. The subsequent induction of Ang II further exacerbates the degeneration of the aortic wall, thereby promoting the occurrence of TAD. Consequently, the combination of BAPN and Ang II represents a refined approach to constructing a murine TAD model, offering a valuable tool to explore the pathogenesis and potential therapeutic approaches for TAD.

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