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Related Experiment Video

Updated: Jun 21, 2026

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm
08:33

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm

Published on: August 24, 2019

Blocking TNF-alpha attenuates aneurysm formation in a murine model.

Wanfen Xiong1, Jason MacTaggart, Rebecca Knispel

  • 1Department of Surgery, University of Nebraska Medical Center, Omaha,NE 68198, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|July 22, 2009
PubMed
Summary

Tumor necrosis factor-alpha (TNF-alpha) drives abdominal aortic aneurysm (AAA) formation by promoting inflammation and matrix degradation. Blocking TNF-alpha with infliximab effectively prevented AAA development in a mouse model.

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Abdominal aortic aneurysm (AAA) involves inflammation and matrix destruction.
  • Macrophages and T lymphocytes infiltrate AAA tissue.
  • Tumor necrosis factor-alpha (TNF-alpha) is elevated in AAA patients.

Purpose of the Study:

  • To investigate the role of TNF-alpha in AAA pathogenesis.
  • To evaluate TNF-alpha antagonism as a therapeutic strategy for AAA.

Main Methods:

  • Utilized a murine model of AAA.
  • Assessed TNF-alpha levels (mRNA and protein) in aneurysm tissue.
  • Examined AAA formation in TNF-alpha deficient mice.
  • Investigated the effect of infliximab (a TNF-alpha antagonist) on AAA growth and associated molecular changes.

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Last Updated: Jun 21, 2026

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm
08:33

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm

Published on: August 24, 2019

A Murine Model of Carotid Aneurysm Formation
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A Murine Model of Carotid Aneurysm Formation

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Porcine Model of Infrarenal Abdominal Aortic Aneurysm
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Porcine Model of Infrarenal Abdominal Aortic Aneurysm

Published on: November 21, 2019

Main Results:

  • TNF-alpha levels were significantly increased in AAA tissue.
  • Mice lacking TNF-alpha were resistant to AAA formation.
  • TNF-alpha deficiency reduced macrophage infiltration and matrix metalloproteinase (MMP) 2 and MMP-9 expression.
  • Infliximab treatment inhibited AAA growth, elastic fiber disruption, macrophage infiltration, and MMP expression.

Conclusions:

  • TNF-alpha plays a critical role in AAA development by regulating inflammation and matrix remodeling.
  • Targeting TNF-alpha with antagonists like infliximab shows therapeutic potential for AAA treatment.