ArticlePloS one2015
Genetics of Plasma Soluble Receptor for Advanced Glycation End-Products and Cardiovascular Outcomes in a Community-based Population: Results from the Atherosclerosis Risk in Communities Study.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Soluble receptor for advanced glycation end products (sRAGE) as a biomarker of COPD.Respiratory research · 2021Pooled it
- Review
- Soluble Receptor for Advanced Glycation End Products and Incident Hypertension in REGARDS.American journal of hypertension · 2025Article
- Soluble receptor for advanced glycation end products and diabetes in Black and White Americans: the REGARDS Study.Obesity medicine · 2025Article
- RAGE/DIAPH1 and atherosclerosis through an evolving lens: Viewing the cell from the "Inside - Out".Atherosclerosis · 2024Review
- The Gly82Ser polymorphism in the receptor for advanced glycation endproducts increases the risk for coronary events in the general population.Scientific reports · 2024Article
- Nanopore Sequencing ofACS omega · 2023Article
- The AGE-RAGE Axis and the Pathophysiology of Multimorbidity in COPD.Journal of clinical medicine · 2023Review
- Polymorphisms and Gene-Gene Interaction in AGER/IL6 Pathway Might Be Associated with Diabetic Ischemic Heart Disease.Journal of personalized medicine · 2022Article
- The Role of Nonenzymatic Post-translational Protein Modifications in Uremic Vascular Calcification.Advances in chronic kidney disease · 2019Review
- The Relationship between the Soluble Receptor for Advanced Glycation End Products and Oxidative Stress in Patients with Palmoplantar Warts.Medicina (Kaunas, Lithuania) · 2019Article
- Pathological Implications of Receptor for Advanced Glycation End-Product (Disease markers · 2019Review
- Clinical and Biological Predictors of Plasma Levels of Soluble RAGE in Critically Ill Patients: Secondary Analysis of a Prospective Multicenter Observational Study.Disease markers · 2018Observational
- Genome-wide association study of 1,5-anhydroglucitol identifies novel genetic loci linked to glucose metabolism.Scientific reports · 2017Article
- Racial differences in circulating levels of the soluble receptor for advanced glycation endproducts in middle-aged and older adults.Metabolism: clinical and experimental · 2017Article
- Cross-sectional Analysis of AGE-CML, sRAGE, and esRAGE with Diabetes and Cardiometabolic Risk Factors in a Community-Based Cohort.Clinical chemistry · 2017Article
- Article
- Novel Risk Factors for Type 2 Diabetes in African-Americans.Current diabetes reports · 2015Review
- Soluble receptor for advanced glycation end products and the risk for incident heart failure: The Atherosclerosis Risk in Communities Study.American heart journal · 2015Article
- Mouse RAGE Variant 4 Is a Dominant Membrane Receptor that Does Not Shed to Generate Soluble RAGE.PloS oneArticle
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Plasma soluble Receptor for Advanced Glycation End-products (sRAGE) is a strong marker of vascular outcomes although evidence on the direction of association is mixed. Compared to whites, blacks have lower levels of sRAGE. We hypothesized that genetic determinants of sRAGE would help clarify the causal role of sRAGE and the black-white difference in sRAGE levels. We conducted a genome-wide analysis of sRAGE in whites and blacks from the Atherosclerosis Risk in Communities Study. Median plasma sRAGE levels were lower in blacks than whites (728 vs. 1067 pg/ml; P<0.0001). The T (vs. C) allele of rs2070600, a missense variant in AGER, the gene encoding RAGE, was associated with approximately 50% lower sRAGE levels in both whites (N = 1,737; P = 7.26x10-16; minor allele frequency (MAF) = 0.04) and blacks (N = 581; P = 0.02; MAF = 0.01). In blacks, the T (vs. C) allele of rs2071288, intronic to AGER, was associated with 43% lower sRAGE levels (P = 2.22x10-8; MAF = 0.10) and was nearly absent in whites. These AGER SNPs explained 21.5% and 26% of the variation in sRAGE in blacks and whites, respectively, but did not explain the black-white difference in sRAGE. These SNPs were not significantly associated with incident death, coronary heart disease, diabetes, heart failure, or chronic kidney disease in whites (N = 8,130-9,017) or blacks (N = 2,293-2,871) (median follow up ~20 years). We identified strong genetic determinants of sRAGE that did not explain the large black-white difference in sRAGE levels or clearly influence risk of clinical outcomes, suggesting that sRAGE may not be a causal factor in development of these outcomes.
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