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Mouse models of atherosclerosis.

C A Reardon¹, G S Getz

¹Department of Pathology, The University of Chicago, Chicago, Illinois 60637, USA.

Current Opinion in Lipidology

|March 27, 2001

Summary

Atherosclerosis, a chronic arterial inflammation, is studied in gene-deficient mice. This review explores genetic factors, lipoproteins, and inflammation

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Area of Science:

Cardiovascular Biology
Immunology
Genetics

Background:

Atherosclerosis is a chronic inflammatory disease affecting arteries.
Apolipoprotein E-deficient and LDL receptor-deficient mice are key models for atherosclerosis research.

Purpose of the Study:

To review the role of genetics and gene products in atherosclerosis development.
To discuss factors influencing atherosclerosis in mouse models, including lipoproteins and inflammation.

Main Methods:

Review of studies utilizing apolipoprotein E-deficient and LDL receptor-deficient mice.
Analysis of genetic modifiers, lipoprotein metabolism, and inflammatory pathways.
Emphasis on examining advanced atherosclerotic lesions and their composition.

Main Results:

Genetics significantly impact atherosclerosis development.
Lipoprotein modifications and receptor interactions are crucial.
Inflammatory gene modifiers and HDL play key roles in atheroprotection.

Conclusions:

Mouse models are valuable for understanding atherosclerosis.
Further research should focus on advanced lesions and detailed composition analysis.

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