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Updated: Apr 28, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
CD36, a scavenger receptor implicated in atherosclerosis.
11] Department of Molecular Medicine, Ewha Womans University School of Medicine, Seoul, Republic of Korea [2] Ewha Global Top 5 Research Program, Ewha Womans University, Seoul, Republic of Korea.
CD36 protein is crucial in atherosclerosis development by mediating oxidized LDL uptake and inflammation. CD36 deficiency significantly reduces atherosclerotic lesion formation, suggesting it as a therapeutic target.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- CD36 is a membrane glycoprotein found on various cells, including macrophages and platelets.
- Macrophage CD36 plays a key role in atherosclerosis by interacting with oxidized low-density lipoprotein (oxLDL).
Purpose of the Study:
- To investigate the multifaceted role of CD36 in the pathogenesis of atherosclerosis.
- To explore CD36's involvement in oxLDL uptake, foam cell formation, and macrophage migration.
Main Methods:
- In vitro studies examining CD36 function in cellular processes.
- In vivo experiments utilizing models to assess CD36's impact on lesion development.
Main Results:
- CD36 facilitates oxLDL uptake and foam cell formation, critical early steps in atherosclerosis.
- Oxidized LDL binding to CD36 inhibits macrophage migration, potentially trapping them in lesions.
- CD36 deficiency was shown to reduce atherosclerotic lesion formation.
- Platelet CD36 contributes to inflammatory processes and thrombus formation post-plaque rupture.
Conclusions:
- CD36 is an essential mediator of atherosclerotic processes, including inflammation and lesion progression.
- Targeting CD36 and its signaling pathways presents a potential therapeutic strategy for atherosclerosis.
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