Impacts of CD36 Variants on Plasma Lipid Levels and the Risk of Early-Onset Coronary Artery Disease: A Systematic

Zhi Luo1, Lingwei Lv2

  • 1Department of Cardiology, Suining Central Hospital, Suining, Sichuan, China.

PubMed

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.

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