ArticleThe Journal of biological chemistry2002
Hypercholesterolemia promotes a CD36-dependent and endothelial nitric-oxide synthase-mediated vascular dysfunction.
Article in The Journal of biological chemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Diversity of Lipid Function in Atherogenesis: A Focus on Endothelial Mechanobiology.International journal of molecular sciences · 2021Review
- Sarcolemmal dependence of cardiac protection and stress-resistance: roles in aged or diseased hearts.British journal of pharmacology · 2016Review
- Alteration of actin dependent signaling pathways associated with membrane microdomains in hyperlipidemia.Proteome science · 2015Article
- MicroRNAs in the onset and development of cardiovascular disease.Clinical science (London, England : 1979) · 2014Review
- Mitral and tufted cells are potential cellular targets of nitration in the olfactory bulb of aged mice.PloS one · 2013Article
- CD36 and Na/K-ATPase-α1 form a proinflammatory signaling loop in kidney.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Novel biological functions of high-density lipoprotein cholesterol.Circulation research · 2012Review
- Role of phospholipid oxidation products in atherosclerosis.Circulation research · 2012Review
- CD36 as a therapeutic target for endothelial dysfunction in stroke.Current pharmaceutical design · 2012Review
- Impact of oxLDL on Cholesterol-Rich Membrane Rafts.Journal of lipids · 2011Article
- Oxidized LDL: diversity, patterns of recognition, and pathophysiology.Antioxidants & redox signaling · 2010Review
- Type 2 scavenger receptor CD36 in platelet activation: the role of hyperlipemia and oxidative stress.Clinical lipidology · 2009Article
- Cholesterol and Kir channels.IUBMB life · 2009Review
- CD36, a scavenger receptor involved in immunity, metabolism, angiogenesis, and behavior.Science signaling · 2009Review
- Enhancing cardiovascular dynamics by inhibition of thrombospondin-1/CD47 signaling.Current drug targets · 2008Review
- oxLDL facilitates flow-induced realignment of aortic endothelial cells.American journal of physiology. Cell physiology · 2008Article
- CD36 deficiency leads to choroidal involution via COX2 down-regulation in rodents.PLoS medicine · 2008Article
- CD36: implications in cardiovascular disease.The international journal of biochemistry & cell biology · 2007Review
- Microarray analysis reveals novel gene expression changes associated with erectile dysfunction in diabetic rats.Physiological genomics · 2005Article
- HDL-associated estradiol stimulates endothelial NO synthase and vasodilation in an SR-BI-dependent manner.The Journal of clinical investigation · 2003Article
Corrections and comments
- Retraction · 2013-03-01Falsification/Fabrication of Image · Investigation by Company/Institution · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · NIH finding of misconduct for Eric J Smart
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- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Numerous studies have implicated either the presence or absence of CD36 in the development of hypertension. In addition, hypercholesterolemia is associated with the loss of nitric oxide-induced vasodilation and the subsequent increase in blood pressure. In the current study, we tested the hypothesis that diet-induced hypercholesterolemia promotes the disruption of agonist-stimulated nitric oxide generation and vasodilation in a CD36-dependent manner. To test this, C57BL/6, apoE null, CD36 null, and apoE/CD36 null mice were maintained on chow or high fat diets. In contrast to apoE null mice fed a chow diet, apoE null mice fed a high fat diet did not respond to acetylcholine with a decrease in blood pressure. Caveolae isolated from in vivo vessels did not contain endothelial nitric-oxide synthase and were depleted of cholesterol. Age-matched apoE/CD36 null mice fed a chow or high fat diet responded to acetylcholine with a decrease in blood pressure. The mechanism underlying the vascular dysfunction was reversible because vessels isolated from apoE null high fat-fed mice regained responsiveness to acetylcholine when incubated with plasma obtained from chow-fed mice. Further analysis demonstrated that the plasma low density lipoprotein fraction was responsible for depleting caveolae of cholesterol, removing endothelial nitric-oxide synthase from caveolae, and preventing nitric oxide production. In addition, the pharmacological removal of caveola cholesterol with cyclodextrin mimicked the effects caused by the low density lipoprotein fraction. We conclude that the ablation of CD36 prevented the negative impact of hypercholesterolemia on agonist-stimulated nitric oxide-mediated vasodilation in apoE null mice. These studies provide a direct link between CD36 and the early events that underlie hypercholesterolemia-mediated hypertension and mechanistic linkages between CD36 function, nitric-oxide synthase activation, caveolae integrity, and blood pressure regulation.
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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.