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Updated: Jul 6, 2026

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Published on: February 7, 2018

Intimal hyperplasia in murine models.

¹Department of Pathology and Laboratory Medicine, Genome Research Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio 45237, USA. huidy@email.uc.edu

Current Drug Targets

|March 14, 2008

Summary

This summary is machine-generated.

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Injury-induced neointimal hyperplasia in mice differs from atherosclerosis. Inflammatory cells like lymphocytes protect against hyperplasia, while monocytes promote it, revealing distinct disease mechanisms.

Area of Science:

Cardiovascular Biology
Immunology
Vascular Biology

Background:

Arterial injury models in mice, such as carotid artery ligation and endothelial denudation, commonly induce neointimal hyperplasia.
Genetic background influences susceptibility to both neointimal hyperplasia and diet-induced atherosclerosis, with distinct strain profiles observed.

Purpose of the Study:

To investigate the differential roles of inflammatory cells and molecular pathways in arterial injury-induced neointimal hyperplasia versus atherosclerosis.
To elucidate the distinct mechanisms underlying neointimal hyperplasia and atherosclerosis despite similar vascular occlusion outcomes.

Main Methods:

Utilized established mouse models of arterial injury (ligation, denudation, periadventitial cuff).
Analyzed the infiltration and function of inflammatory cells (lymphocytes, monocytes, macrophages) at injury sites.

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Last Updated: Jul 6, 2026

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

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Published on: February 7, 2018

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

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Published on: May 14, 2014

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Assessed the role of specific cytokines (interferon-gamma, tumor necrosis factor-alpha) and inducible nitric oxide synthase (iNOS) activity.

Main Results:

T and B lymphocytes were found to be protective against injury-induced neointimal hyperplasia, contrasting their role in atherosclerosis.
Monocyte infiltration and differentiation into macrophages promoted neointimal hyperplasia.
Inducible nitric oxide synthase (iNOS) exhibited context-dependent effects, inhibiting hyperplasia in denudation models but promoting it with cuff placement.

Conclusions:

Neointimal hyperplasia and atherosclerosis, despite causing similar vascular occlusion, possess distinct pathological mechanisms.
The cellular and molecular responses to arterial injury differ significantly from those in diet-induced atherosclerosis, particularly regarding inflammatory cell involvement.
Understanding these differences is crucial for developing targeted therapeutic strategies for vascular diseases.