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The role of CD36 in cardiovascular disease
Hongyang Shu1,2, Yizhong Peng3, Weijian Hang1,2
1Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, China.
Insights
CD36, a receptor crucial for fatty acid uptake in the heart, is implicated in cardiovascular diseases. Modulating CD36 levels may offer a novel therapeutic strategy for conditions like diabetic cardiomyopathy and atherosclerosis.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- CD36 (scavenger receptor B2) is vital for long-chain fatty acid uptake in myocardial tissue.
- Its maturation and transport involve post-translational modifications like phosphorylation and glycosylation.
- CD36 expression varies in cardiovascular pathologies, being decreased in ischemia-reperfusion and pressure overload, but increased in diabetic cardiomyopathy and atherosclerosis.
Purpose of the Study:
- To review the regulation and post-translational modifications of CD36.
- To evaluate the role of CD36 in cardiovascular diseases.
- To assess the potential of CD36 as a therapeutic target.
Main Methods:
- Literature review of studies on CD36.
- Analysis of CD36 expression patterns in various cardiovascular conditions.
- Evaluation of experimental data on CD36 deficiency and overexpression in disease models.
Main Results:
- CD36 deficiency ameliorates diabetic cardiomyopathy and atherosclerosis.
- CD36 overexpression protects against ischemia-reperfusion injury.
- These findings highlight CD36's significant association with cardiovascular disease progression.
Conclusions:
- CD36 plays a critical role in cardiovascular pathophysiology.
- Targeting CD36 presents a promising therapeutic avenue for cardiovascular diseases.
- Further research into CD36 regulation and function is warranted.
Abstract:
CD36, also known as the scavenger receptor B2, is a multifunctional receptor widely expressed in various organs. CD36 plays a crucial role in the uptake of long-chain fatty acids, the main metabolic substrate in myocardial tissue. The maturation and transportation of CD36 is regulated by post-translational modifications, including phosphorylation, ubiquitination, glycosylation, and palmitoylation. CD36 is decreased in pathological cardiac hypertrophy caused by ischaemia-reperfusion and pressure overload, and increased in diabetic cardiomyopathy and atherosclerosis. Deficiency of CD36 alleviates diabetic cardiomyopathy and atherosclerosis, while overexpression of CD36 eliminates ischaemia-reperfusion damage, together suggesting that CD36 is closely associated with the progression of cardiovascular diseases and may be a new therapeutic target. This review summarizes the regulation and post-translational modifications of CD36 and evaluates its role in cardiovascular diseases and its potential as a therapeutic target.
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