{"title":"Impacts of CD36 Variants on Plasma Lipid Levels and the Risk of Early-Onset Coronary Artery Disease: A Systematic Review and Meta-Analysis","authors":"Zhi Luo, Lingwei Lv","doi":"10.1155/cdr/8098173","DOIUrl":null,"url":null,"abstract":"<p><b>Background:</b> 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 <i>CD36</i> gene variants on lipid profiles and EOCAD risk.</p><p><b>Methods:</b> PubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until June 15, 2024.</p><p><b>Results:</b> 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.</p><p><b>Conclusions:</b> The rs1761667, rs1049673, and rs3211956 variants of the <i>CD36</i> gene have significant impacts on lipid levels and may serve as genetic markers for the risk of EOCAD primarily in Chinese. The impacts of <i>CD36</i> variants on EOCAD risk are mediated, at least partly, by dyslipidemia. Genetic screening of <i>CD36</i> gene variants may be helpful for early intervention or prevention of EOCAD in individuals with high risk factors.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8098173","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiovascular Therapeutics","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1155/cdr/8098173","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged.
Subject areas include (but are by no means limited to):
Acute coronary syndrome
Arrhythmias
Atherosclerosis
Basic cardiac electrophysiology
Cardiac catheterization
Cardiac remodeling
Coagulation and thrombosis
Diabetic cardiovascular disease
Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF)
Hyperlipidemia
Hypertension
Ischemic heart disease
Vascular biology
Ventricular assist devices
Molecular cardio-biology
Myocardial regeneration
Lipoprotein metabolism
Radial artery access
Percutaneous coronary intervention
Transcatheter aortic and mitral valve replacement.