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Published on: June 12, 2019
CD36 and lipid metabolism in the evolution of atherosclerosis
Lei Zhao1, Z Varghese2, J F Moorhead2
1Centre for Lipid Research & Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Insights
CD36, a scavenger receptor, plays a complex role in atherosclerosis. Both too much and too little CD36 increase atherosclerosis risk, suggesting an optimal expression level is crucial.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Research
Background:
- CD36 is a scavenger receptor involved in lipid homeostasis and immune responses.
- It is closely linked to atherosclerosis development and progression.
Purpose of the Study:
- To review the dual role of CD36 in atherosclerosis.
- To explore potential therapeutic strategies targeting CD36.
Main Methods:
- Literature review of academic articles.
Main Results:
- Both CD36 up-regulation and deficiency are associated with increased atherosclerosis risk.
- Abnormal CD36 expression contributes to inflammation, foam cell formation, and thrombosis.
- CD36 deficiency can lead to dyslipidemia and metabolic disorders.
Conclusions:
- An optimal CD36 expression level may be protective against atherosclerosis.
- Targeting CD36 at the post-translational level presents a promising therapeutic avenue.
Background:
CD36 is a multi-functional class B scavenger receptor, which acts as an important modulator of lipid homeostasis and immune responses.
Sources Of Data:
This review uses academic articles.
Areas Of Agreement:
CD36 is closely related to the development and progression of atherosclerosis.
Areas Of Controversy:
Both persistent up-regulation of CD36 and deficiency of CD36 increase the risk for atherosclerosis. Abnormally up-regulated CD36 promotes inflammation, foam cell formation, endothelial apoptosis, macrophage trapping and thrombosis. However, CD36 deficiency also causes dyslipidemia, subclinical inflammation and metabolic disorders, which are established risk factors for atherosclerosis.
Growing Points:
There may be an 'optimal protective window' of CD36 expression.
Areas Timely For Developing Research:
In addition to traditionally modulating protein functions using gene overexpression or deficiency, the modulation of CD36 function at post-translational levels has recently been suggested to be a potential therapeutic strategy.
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