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Isolation and Analysis of Aortic Arch and Root Lesions in an Atherosclerotic Mouse Model
Published on: February 14, 2025
FXR deficiency causes reduced atherosclerosis in Ldlr-/- mice
Yanqiao Zhang1, Xuping Wang, Charisse Vales
1Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA. yqzhang@mednet.ucla.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|July 11, 2006
Summary
FXR deficiency in male mice reduces atherosclerosis by lowering LDL cholesterol and macrophage CD36 expression. This finding offers insights into atherosclerosis development and potential therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Metabolic Diseases
- Molecular Genetics
Background:
- The Farnesoid X Receptor (FXR) plays a role in lipid metabolism.
- FXR knockout (Fxr-/-) mice display a proatherogenic lipoprotein profile.
- Understanding FXR's role in atherosclerosis is crucial for metabolic disease research.
Purpose of the Study:
- To investigate the role of FXR in the development of atherosclerosis.
- To determine if FXR deficiency impacts lesion development in a mouse model.
- To explore the mechanisms underlying FXR's influence on atherosclerosis.
Main Methods:
- Generated Fxr-/- Ldlr-/- (DKO) mice to study atherosclerosis.
- Administered a Western diet to DKO and Ldlr-/- mice for 16 weeks.
- Analyzed atherosclerotic lesion size, plasma lipid levels, and macrophage gene expression.
Main Results:
- Male DKO mice exhibited reduced atherosclerotic lesions compared to Ldlr-/- mice.
- DKO mice showed decreased plasma LDL and HDL cholesterol, with a 4-fold increase in triglycerides.
- Macrophages from DKO mice displayed reduced CD36 mRNA expression and neutral lipid accumulation.
Conclusions:
- FXR deficiency in male Ldlr-/- mice reduces aortic atherosclerotic lesion size.
- This reduction is associated with decreased plasma LDL cholesterol and diminished macrophage CD36 expression.
- FXR's role in atherosclerosis is sex-dependent, impacting lipid metabolism and macrophage function.
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