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Updated: Dec 12, 2025
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications
Kunming Tian1, Yan Xu2, Amirhossein Sahebkar3,4,5
1Department of Preventive Medicine, School of Public Health, Zunyi Medical University, Zunyi, Guizhou, China. nonstandstill@163.com.
Insights
CD36 (scavenger receptor) plays a key role in atherosclerosis by mediating lipid uptake and inflammation. Targeting CD36 offers potential therapeutic strategies for this chronic cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Immunology
- Metabolic Disease
Background:
- Atherosclerosis involves lipid retention and inflammation in artery walls, driven by modified low-density lipoprotein (LDL).
- Oxidized LDL (ox-LDL) uptake by cells via scavenger receptors like CD36 is critical in plaque development.
- CD36 is a scavenger receptor and signaling hub involved in lipid and inflammatory pathways.
Purpose of the Study:
- To review the structure, ligands, functions, and regulation of CD36 in atherosclerosis.
- To focus on the pathological role of CD36 in endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets.
- To highlight therapeutic strategies targeting CD36 for atherosclerosis.
Main Methods:
- State-of-the-art literature review.
- Analysis of CD36's role in cellular dysfunction.
- Examination of CD36's involvement in lipid and inflammatory pathways.
Main Results:
- CD36 deficiency in mice suggests a protective role against atherosclerosis.
- Soluble CD36 levels are elevated in patients with atherosclerosis and metabolic disorders.
- CD36 mediates ox-LDL uptake and contributes to cellular dysfunction in atherosclerosis.
Conclusions:
- CD36 is a significant contributor to atherosclerotic plaque formation and progression.
- Targeting CD36 expression or activity presents a promising therapeutic avenue for atherosclerosis.
- Further research into CD36's multifaceted roles can advance cardiovascular disease treatment.
Purpose Of Review:
Atherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein.
Recent Findings:
Animal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders. We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis.
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