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Updated: Mar 29, 2026

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

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Study on the Role and Mechanism of TOPORS in Regulating Aortic Dissection by Mediating SUMOylation

Yuan Hu1,2, Luxi Yang2, Wenjun Zhou1,2

  • 1The First Clinical Medical College, Lanzhou University, Lanzhou 730099, China.

Journal of Cardiovascular Development and Disease
|March 27, 2026
PubMed

Insights

TOPORS exacerbates aortic dissection (AD) by activating p53 and inhibiting PI3K/AKT signaling through SUMOylation. Reducing TOPORS alleviates AD progression, offering a potential therapeutic target for this cardiovascular emergency.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pathogenesis of Aortic Dissection

Background:

  • Aortic dissection (AD) is a life-threatening cardiovascular emergency.
  • The role of SUMOylation, particularly via TOPORS, in AD pathogenesis is not well understood.
  • Understanding molecular mechanisms underlying AD is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of TOPORS in regulating AD pathogenesis through SUMOylation.
  • To elucidate the molecular pathways influenced by TOPORS in AD.
  • To assess the therapeutic potential of targeting TOPORS in AD.

Main Methods:

  • Analysis of TOPORS expression in human AD and normal aortic tissues.
  • In vivo (mouse models) and in vitro (VSMC models) experiments to study TOPORS function.
  • Assessment of inflammatory cytokine secretion, PI3K/AKT and p53 signaling pathways, and SUMOylation of p53.

Main Results:

  • TOPORS expression was significantly upregulated in AD tissues.
  • Inhibition of TOPORS ameliorated aortic dilation, elastic fiber degradation, and inflammatory cytokine secretion.
  • TOPORS knockout promoted PI3K/AKT phosphorylation, downregulated p53 signaling, and reduced p53 SUMOylation, thereby decreasing VSMC apoptosis and inflammation.

Conclusions:

  • TOPORS plays a critical role in AD pathogenesis by activating p53 and inhibiting PI3K/AKT phosphorylation via SUMOylation.
  • Targeting TOPORS may represent a novel therapeutic strategy for managing aortic dissection.
  • This study provides new insights into the molecular mechanisms driving AD progression.

Keywords:
SUMOylationTOPORSVSMCaortic dissectionp53

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