CD36, originally identified as glycoprotein IV on platelets, is an 88-kDa integral membrane protein that has multiple ligands and is expressed in the cardiovascular system (ie, blood vessel walls and the heart). Human genetic CD36 deficiency is relatively frequent in Asian and African populations. Investigation into the pathophysiology of this disorder has shown that CD36 may play an important role as a major scavenger receptor for oxidized low-density lipoproteins and as a crucial transporter for long-chain fatty acids. The CD36 deficiency may be related to the phenotypic expression of the "metabolic syndrome," which is frequently associated with atherosclerotic cardiovascular diseases. It also has been reported that CD36 deficiency might be linked with cardiomyopathy. These data raised the possibility that CD36 deficiency might be an important genetic background for these life-threatening human cardiovascular diseases.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s1050-1738(03)00026-4 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CD36 Deficiency.
QJM
December 2024
Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Microvascular insulin resistance with enhanced muscle glucose disposal in CD36 deficiency.
Diabetologia
November 2024
Department of Medicine, Division of Nutritional Sciences and Obesity Research, Washington University School of Medicine, St Louis, MO, USA.
Article Synopsis
- Microvascular dysfunction contributes to insulin resistance, particularly in individuals with a genetic variant (G allele) that reduces CD36 expression, impacting blood vessel function and glucose disposal.* -
- Through various experimental methods, the study found that while CD36-deficient mice and humans showed improved insulin-stimulated glucose disposal, they had issues with blood volume response and vascular compliance, indicating a paradoxical relationship between microvascular resistance and insulin sensitivity.* -
- The findings suggest that while CD36 deficiency may enhance glucose disposal efficiency, it simultaneously hampers the microvasculature's response to insulin, affecting oxygen delivery and energy metabolism in muscle and heart tissues.*
CD36 deficiency protects lipopolysaccharide-induced sepsis via inhibiting CerS6-mediated endoplasmic reticulum stress.
Int Immunopharmacol
December 2024
Department of Biochemistry, Chung-Ang University College of Medicine, Seoul 06974, Republic of Korea. Electronic address:
The type 2 scavenger receptor CD36 functions not only as a long chain fatty acid transporter, but also as a pro-inflammatory mediator. Ceramide is the simple N-acylated form of sphingosine and exerts distinct biological activity depending on its acyl chain length. Six ceramide synthases (CerS) in mammals determine the chain length of ceramide species, and CerS6 mainly produces C16-ceramide.
View Article and Find Full Text PDFHaplotypes analysis reveals the genetic basis of type I CD36 deficiency.
Sci Rep
October 2024
Institute of Blood Transfusion and Hematology, Guangzhou Blood Center, Guangzhou Medical University, Guangzhou, China.
CD36, also known as glycoprotein IV, is classified into two distinct subgroups based on the presence or absence of its expression on monocytes. The CD36 gene spans approximately 50,000 base pairs. Historically, research has focused on identifying CD36 mutations through Sanger sequencing and next-generation sequencing (NGS), with limited exploration of haplotypes.
View Article and Find Full Text PDFCD36 restricts lipid-associated macrophages accumulation in white adipose tissues during atherogenesis.
Front Cardiovasc Med
August 2024
Versiti Blood Research Institute, Milwaukee, WI, United States.
Visceral white adipose tissues (WAT) regulate systemic lipid metabolism and inflammation. Dysfunctional WAT drive chronic inflammation and facilitate atherosclerosis. Adipose tissue-associated macrophages (ATM) are the predominant immune cells in WAT, but their heterogeneity and phenotypes are poorly defined during atherogenesis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!