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Published on: February 20, 2019
Is the suppression of CD36 a promising way for atherosclerosis therapy?
Shi-Yuan Wen1, Xiaoyan Zhi1, Hai-Xin Liu2
1College of Basic Medical Sciences, Shanxi Medical University, Taiyuan, China.
Insights
Atherosclerosis, a cardiovascular disease, involves plaque buildup. Targeting CD36, a key lipid regulator, offers a promising therapeutic strategy for preventing and treating this condition.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Pharmacology
Background:
- Atherosclerosis is a primary cause of cardiovascular diseases, characterized by arterial plaque formation and posing a global health threat.
- CD36 is a critical regulator of lipid homeostasis, implicated in atherosclerosis development and progression, making it a potential therapeutic target.
- Abnormal CD36 overexpression contributes to lipid accumulation, foam cell formation, inflammation, endothelial apoptosis, and thrombosis.
Purpose of the Study:
- To review the structure, expression regulation, and function of CD36 in atherosclerosis.
- To explore pharmacological therapies targeting CD36 for atherosclerosis prevention and treatment.
- To highlight the significance of CD36 suppression strategies for developing novel anti-atherosclerotic drugs.
Main Methods:
- Literature review of studies on CD36 structure, function, and regulation in atherosclerosis.
- Analysis of research on natural products and lipid-lowering agents targeting CD36.
- Examination of preclinical and clinical data on CD36-targeted therapies.
Main Results:
- CD36 plays a central role in key pathological processes of atherosclerosis.
- Numerous agents targeting CD36 suppression or upregulation inhibition show potential in preventing and treating atherosclerosis.
- Targeting CD36 is a viable strategy for developing new therapeutic interventions.
Conclusions:
- CD36 is a significant therapeutic target for atherosclerosis.
- Strategies aimed at CD36 suppression are crucial for developing effective anti-atherosclerotic drugs.
- Further research into CD36-targeted therapies holds promise for clinical applications in cardiovascular disease management.
Abstract:
Atherosclerosis is the main underlying pathology of many cardiovascular diseases and is marked by plaque formation in the artery wall. It has posed a serious threat to the health of people all over the world. CD36 acts as a significant regulator of lipid homeostasis, which is closely associated with the onset and progression of atherosclerosis and may be a new therapeutic target. The abnormal overexpression of CD36 facilitates lipid accumulation, foam cell formation, inflammation, endothelial apoptosis, and thrombosis. Numerous natural products and lipid-lowering agents are found to target the suppression of CD36 or inhibit the upregulation of CD36 to prevent and treat atherosclerosis. Here, the structure, expression regulation and function of CD36 in atherosclerosis and its related pharmacological therapies are reviewed. This review highlights the importance of drugs targeting CD36 suppression in the treatment and prevention of atherosclerosis, in order to develop new therapeutic strategies and potential anti-atherosclerotic drugs both preclinically and clinically.
