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Aneurysm management involves either conservative medical therapy or surgical intervention, depending on the size and symptoms of the aneurysm. Conservative management is generally reserved for smaller, asymptomatic aneurysms, while larger or symptomatic aneurysms often necessitate surgical repair.Conservative Medical TherapyFor small, asymptomatic aneurysms, particularly abdominal aortic aneurysms (AAA) less than 5.5 centimeters in diameter, conservative medical therapy is recommended. This...
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Updated: Nov 15, 2025

Creation of a Rodent Model of Abdominal Aortic Aneurysm by Blocking Adventitial Vasa Vasorum Perfusion
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Time-Dependent Pathological Changes in Hypoperfusion-Induced Abdominal Aortic Aneurysm.

Hirona Kugo1, Wanida Sukketsiri2, Hiroki Tanaka3

  • 1Department of Applied Biological Chemistry, Graduate School of Agriculture, Kindai University, 204-3327 Nakamachi, Nara 631-8505, Japan.

Biology
|March 6, 2021
PubMed
Summary

Hypoperfusion causes aortic wall hypoxia, contributing to abdominal aortic aneurysm (AAA) development. This study details the time-dependent pathological cascade of AAA formation, revealing early impacts on smooth muscle cells.

Keywords:
abdominal aortic aneurysmhypoperfusionhypoxiainflammationvascular disease

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Area of Science:

  • Cardiovascular pathology
  • Vascular biology
  • Atherosclerosis research

Background:

  • Hypoperfusion via vasa vasorum stenosis can induce aortic wall hypoxia, a key factor in abdominal aortic aneurysm (AAA) development.
  • The precise correlation between hypoperfusion and the pathological mechanisms of AAA remains incompletely understood.

Purpose of the Study:

  • To perform a time-dependent pathological analysis of hypoperfusion-induced aortic wall changes.
  • To elucidate the mechanisms underlying gradual aortic wall degradation leading to AAA formation.
  • To identify and group AAA-related factors based on their dynamic changes over time.

Main Methods:

  • Semi-quantitative pathological analysis of aortic wall changes over time.
  • Categorization of AAA-related factors into five distinct temporal groups.
  • Evaluation of factors including angiotensin II type 1 receptor, endothelin-1 (ET-1), malondialdehyde (MDA), matrix metalloproteinases (MMPs), macrophage markers (Mac387+, CD163+), monocyte chemotactic protein-1, smooth muscle cell (SMC) phenotypes, neutrophil elastase, and angiotensinogen.

Main Results:

  • Hypoxia-inducible factor-1α, ET-1, MDA, and MMP-9 were found to colocalize with alpha-smooth muscle actin cells within 3 hours.
  • This early colocalization suggests that hypoperfusion-induced hypoxia directly impacts contractile SMC activity in the initial stages of AAA.
  • The study successfully clarified the temporal cascade of various AAA-related factors.

Conclusions:

  • The time-dependent analysis provides critical insights into the multistage pathological processes involved in AAA development.
  • Findings highlight the direct effect of hypoperfusion-induced hypoxia on vascular smooth muscle cells early in AAA pathogenesis.
  • This research offers a foundation for understanding the complex sequence of events leading to AAA.