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Updated: Aug 5, 2026

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The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury
Published on: October 3, 2017
LAMB2 p.E991K Mutation-Mediated Atherosclerosis in Rabbit
Ronghan Zhang1, Chao Mu1, Shujun Yang1
1Key Lab for Zoonosis Research, College of Veterinary Medicine, Jilin University, Changchun 130062, China.
Genes
|July 28, 2026
Summary
The LAMB2 p.E991K mutation exacerbates atherosclerosis by disrupting basement membrane integrity, increasing inflammation, and altering lipid metabolism. This highlights LAMB2 as a key genetic factor influencing cardiovascular disease risk.
Area of Science:
- Genetics
- Cardiovascular Biology
- Molecular Medicine
Background:
- Atherosclerosis is a primary cause of cardiovascular disease, influenced by genetic and environmental factors.
- The LAMB2 p.E987K variant is linked to atherosclerosis susceptibility, but its functional role is unknown.
Purpose of the Study:
- To investigate the functional role of the LAMB2 p.E991K mutation in atherosclerosis development.
Main Methods:
- Generated a rabbit model with the LAMB2 p.E991K mutation using CRISPR/Cas9-SpG.
- Induced atherosclerosis using a high-fat diet (HFD).
- Analyzed lipid accumulation, plaque size, cellular markers, LAMB2 expression, basement membrane integrity, and inflammasome activation.
Main Results:
- LAMB2 mutant rabbits showed increased body weight, lipid abnormalities, and larger aortic atherosclerotic plaques.
- Reduced alpha-smooth muscle actin (α-SMA) and elevated CD4/MCP-1 indicated smooth muscle cell loss and immune dysregulation.
- Decreased LAMB2 expression, basement membrane disruption, and NLRP3 inflammasome activation were observed.
Conclusions:
- The LAMB2 p.E991K mutation promotes HFD-induced atherosclerosis by impairing basement membrane integrity, enhancing inflammation, and disrupting lipid metabolism.
- LAMB2 acts as a genetic modifier influencing atherosclerosis susceptibility.
