ArticleJournal of clinical laboratory analysis2022
Genetic variants, gene expression, and soluble CD36 analysis in acute coronary syndrome: Differential protein concentration between ST-segment elevation myocardial infarction and unstable angina.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Lipoprotein(a)/CD36 Interaction Drives IL-6/RhoA-GTP Signaling and miRNA Epigenetic Regulation in Coronary Artery Spasm.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Association of oxidized ApoB and oxidized ApoA-I with high-risk coronary plaque features in cardiovascular disease.JCI insight · 2023Observational
- The association of soluble cluster of differentiation 36 with metabolic diseases: A potential biomarker and therapeutic target.Pediatric discovery · 2023Review
- Prognostic Value of the Selected Polymorphisms in theBiomedicines · 2023Article
- Scavenger Receptors in Myocardial Infarction and Ischemia/Reperfusion Injury: The Potential for Disease Evaluation and Therapy.Journal of the American Heart Association · 2023Review
- Genetic variants, gene expression, and soluble CD36 analysis in acute coronary syndrome: Differential protein concentration between ST-segment elevation myocardial infarction and unstable angina.Journal of clinical laboratory analysis · 2022Article
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis plays an important role in the pathophysiology of acute coronary syndrome (ACS). CD36 is a scavenger receptor involved in lipid metabolism. Some single-nucleotide variants in the non-coding region could indirectly alter the expression and the function of the protein.
objectiveThe aim of this study was to investigate the gene and protein expression associated with CD36 variants (rs1194182;C > G; rs1049654;C > A, rs1334512;G > T, and rs3211892;G > A) in ACS patients from the western Mexican population.
methodsWe recruited 310 ACS patients and 308 subjects in the control group (CG). Genotyping was determined by TaqMan SNP genotyping assays. CD36 expression at the mRNA level was quantified by TaqMan gene expression assays. Soluble CD36 (sCD36) was measured by enzyme-linked immunosorbent assay.
resultsWe show that rs1194182G > C variant provides a protective effect with a 1.7-fold lower susceptibility to develop ACS (p = 0.03); however, this association was masked by diabetes and dyslipidemia. We observed a higher sCD36 concentration in patient with ST-segment elevation myocardial infarction (STEMI) compared with patients with unstable angina (UA) (p = 0.038). Likewise, in diabetic patients versus non-diabetic (p < 0.001). We observed in patients an increase in CD36 mRNA expression (1.91 times higher) than in the CG (p = 0.02).
conclusionThe rs1194182 seems to be associated with diabetes in a risky manner, in ACS patients and protective for dyslipidemia in both groups. The concentration of sCD36 seems to be associated with the clinical spectrum of the ACS patients and the presence of diabetes, since patients with STEMI present significantly elevated level compared with UA.
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