Trial reportThe Journal of clinical endocrinology and metabolism2016
A Common CD36 Variant Influences Endothelial Function and Response to Treatment with Phosphodiesterase 5 Inhibition.
Trial report in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Microvascular insulin resistance with enhanced muscle glucose disposal in CD36 deficiency.Diabetologia · 2025Trial
- Endosomal Mechanisms in Heart Failure Pathophysiology.Current heart failure reports · 2025Review
- Fatty Acid Transport and Signaling: Mechanisms and Physiological Implications.Annual review of physiology · 2023Review
- Cardiac immune cell infiltration associates with abnormal lipid metabolism.Frontiers in cardiovascular medicine · 2022Article
- Visceral obesity and insulin resistance associate with CD36 deletion in lymphatic endothelial cells.Nature communications · 2021Article
- Endothelial Cell Receptors in Tissue Lipid Uptake and Metabolism.Circulation research · 2021Review
- Multi-Ethnic Genome-Wide Association Study of Decomposed Cardioelectric Phenotypes Illustrates Strategies to Identify and Characterize Evidence of Shared Genetic Effects for Complex Traits.Circulation. Genomic and precision medicine · 2020Article
- Effect of a phosphodiesterase-5A (PDE5A) gene polymorphism on response to sildenafil therapy in canine pulmonary hypertension.Scientific reports · 2019Article
- CD36 Modulates Fasting and Preabsorptive Hormone and Bile Acid Levels.The Journal of clinical endocrinology and metabolism · 2018Article
- Intestinal CD36 and Other Key Proteins of Lipid Utilization: Role in Absorption and Gut Homeostasis.Comprehensive Physiology · 2018Review
- Towards Precision Medicine for Hypertension: A Review of Genomic, Epigenomic, and Microbiomic Effects on Blood Pressure in Experimental Rat Models and Humans.Physiological reviews · 2017Review
- CD36 deficiency impairs the small intestinal barrier and induces subclinical inflammation in mice.Cellular and molecular gastroenterology and hepatology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
contextThe scavenger receptor CD36 influences the endothelial nitric oxide-cGMP pathway in vitro. Genetic variants that alter CD36 level are common in African Americans (AAs), a population at high risk of endothelial dysfunction.
objectiveTo examine if the minor allele (G) of coding CD36 variant rs3211938 (G/T) which reduces CD36 level by approximately 50% influences endothelial function, insulin sensitivity (IS), and the response to treatment with the nitric oxide-cGMP potentiator sildenafil.
designIS (frequently sampled iv glucose tolerance) and endothelial function (flow mediated dilation [FMD]) were determined in age- and body mass index-matched obese AA women with or without the G allele of rs3211938 (protocol 1). Effect of chronic sildenafil treatment on IS and FMD was tested in AA women with metabolic syndrome and with/without the CD36 variant, using a randomized, placebo-controlled trial (protocol 2).
settingTwo-center study.
participantsObese AA women.
interventionA total of 20-mg sildenafil citrate or placebo thrice daily for 4 weeks. MAIN OUTCOME: IS, FMD.
resultsG allele carriers have lower FMD (P = .03) and cGMP levels (P = .01) than noncarriers. Sildenafil did not improve IS, mean difference 0.12 (95% confidence interval [CI], -0.33 to 0.58; P = .550). However, there was a significant interaction between FMD response to sildenafil and rs3211938 (P = .018). FMD tended to improve in G carriers, 2.9 (95% CI, -0.9 to 6.8; P = .126), whereas it deteriorated in noncarriers, -2.6 (95% CI, -5.1 to -0.1; P = .04).
conclusionsThe data document influence of a common genetic variant on susceptibility to endothelial dysfunction and its response to sildenafil treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.