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Updated: Jun 16, 2026
06:59
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
CD137 (4-1BB) deficiency reduces atherosclerosis in hyperlipidemic mice
Hyung Jun Jeon1, Jae-Hoon Choi, In-Hyuk Jung
1Division of Life and Pharmaceutical Science, Ewha Womans University, Seoul, Korea.
Circulation
|February 24, 2010
Summary
Blocking CD137 (4-1BB) signaling reduces atherosclerosis progression. This pathway promotes inflammatory molecules and cytokines, contributing to plaque formation. Targeting CD137 offers a promising therapeutic strategy for atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Biology
- Molecular Medicine
Background:
- The tumor necrosis factor receptor superfamily is implicated in atherosclerosis.
- CD137 (4-1BB) is present in atherosclerotic lesions, but its specific role is unclear.
- Understanding CD137's function is crucial for developing atherosclerosis therapies.
Purpose of the Study:
- To investigate the role of CD137 in atherosclerosis development.
- To determine the effects of blocking CD137/CD137 ligand signaling on lesion formation.
Main Methods:
- Generated CD137-deficient apolipoprotein E-knockout (ApoE(-/-) CD137(-/-)) and LDL-receptor-knockout (Ldlr(-/-)CD137(-/-)) mice.
- Analyzed atherosclerotic plaque size and inflammatory markers.
Main Results:
- CD137 deficiency reduced atherosclerotic plaque lesions in both mouse models.
- Reduced lesions correlated with decreased levels of interferon-gamma, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha.
- CD137 signaling upregulated inflammatory molecules (MCP-1, IL-6, VCAM-1, ICAM-1) in endothelial cells and activated monocytes/macrophages.
Conclusions:
- CD137/CD137 ligand signaling plays a significant role in atherosclerosis progression.
- Blocking the CD137 pathway is a potential therapeutic target for treating atherosclerosis.
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