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Impacts of CD36 Variants on Plasma Lipid Levels and the Risk of Early-Onset Coronary Artery Disease: A Systematic
1Department of Cardiology, Suining Central Hospital, Suining, Sichuan, China.
Insights
Specific variants in the CD36 gene impact lipid levels and early-onset coronary artery disease (EOCAD) risk. Genetic screening of these CD36 variants may aid in preventing EOCAD in high-risk individuals.
Area of Science:
- Genetics and Molecular Biology
- Cardiovascular Disease Research
- Metabolic Disorders
Background:
- Cluster of differentiation 36 (CD36) is implicated in dyslipidemia and early-onset coronary artery disease (EOCAD).
- Investigating the influence of CD36 gene variants on lipid profiles and EOCAD risk is crucial for understanding disease mechanisms.
- Dyslipidemia is a significant risk factor for cardiovascular diseases, including EOCAD.
Approach:
- A comprehensive literature search was conducted across major databases (PubMed, Cochrane Library, Central, CINAHL, ClinicalTrials.gov) up to June 15, 2024.
- Meta-analysis of 25 studies involving 11,494 individuals was performed to assess the association between CD36 variants, lipid levels, and EOCAD risk.
- Subgroup analysis focused on specific ethnic populations to identify potential variations in genetic associations.
Key Points:
- The rs1761667 variant of CD36 was associated with higher high-density lipoprotein cholesterol (HDL-C) and increased EOCAD risk.
- The rs1049673 and rs3211956 variants were linked to lower low-density lipoprotein cholesterol (LDL-C) and reduced EOCAD risk.
- Antiatherosclerotic effects and reduced EOCAD risk were notably observed in Chinese individuals carrying rs1049673 and rs3211956 variants.
Conclusions:
- CD36 gene variants rs1761667, rs1049673, and rs3211956 significantly affect lipid profiles and may serve as genetic markers for EOCAD risk, particularly in the Chinese population.
- The association between CD36 variants and EOCAD risk is partly mediated by dyslipidemia.
- Genetic screening of CD36 variants could facilitate early intervention and prevention strategies for EOCAD in individuals with risk factors.
Abstract:
Background: Recent studies have indicated that cluster of differentiation 36 (CD36) is closely linked to dyslipidemia and early-onset coronary artery disease (EOCAD). This study is aimed at investigating the impacts of CD36 gene variants on lipid profiles and EOCAD risk. Methods: PubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until June 15, 2024. Results: In total, 25 studies (11,494 individuals) were included for the analysis. The A allele carriers of the rs1761667 variant had higher high-density lipoprotein cholesterol (HDL-C) levels and higher EOCAD risk than noncarriers. In contrast, the G allele carriers of the rs1049673 and rs3211956 variants had lower low-density lipoprotein cholesterol (LDL-C) levels and lower EOCAD risk than noncarriers. Subgroup analysis indicated that the antiatherosclerotic impact and reduced EOCAD risk were primarily observed in Chinese with rs1049673 and rs3211956. Conclusions: The rs1761667, rs1049673, and rs3211956 variants of the CD36 gene have significant impacts on lipid levels and may serve as genetic markers for the risk of EOCAD primarily in Chinese. The impacts of CD36 variants on EOCAD risk are mediated, at least partly, by dyslipidemia. Genetic screening of CD36 gene variants may be helpful for early intervention or prevention of EOCAD in individuals with high risk factors.
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