ArticleCirculation research2014
Ceramide changes the mediator of flow-induced vasodilation from nitric oxide to hydrogen peroxide in the human microcirculation.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05107869 (Effect of Plasma Ceramides on Peripheral Vascular Function), which is not on this map. Cited by 96 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.
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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.
Effect of Plasma Ceramides on Peripheral Vascular Function
Who cites it
96 citing papers in PubMed, 138 citations in OpenAlex.
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- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
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- Disruption of sphingolipid metabolism triggers lung vascular inflammation and aging-like changes under hypoxia through VDAC1-mediated mitochondrial DNA release.Apoptosis : an international journal on programmed cell death · 2026Article
- Chronic Kidney Disease, Circulating Ceramides, and Coronary Microvascular Dysfunction: Insights from the CRUISE-MET Study.Cardiorenal medicine · 2026Observational
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
- Microvascular Reactivity to Cutaneous Local Heating in the Paretic and Non-Paretic Legs of Chronic Stroke Survivors-A Pilot Study.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Estrogen Influences Human Microvascular Endothelial Function Via Sex-Specific Regulation of Sphingolipids.JACC. Basic to translational science · 2026Article
- Characterization of anticancer therapy-induced microvascular dysfunction in patients with breast cancer supports targeted intervention.JCI insight · 2025Article
- Ceramide as a Biomarker for HFpEF in Women: Menopause, Aging, and Pregnancy.International journal of molecular sciences · 2025Review
- Cystathionine γ lyase deletion enhances corpus cavernosum contraction via thromboxane AAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Obesity-Associated Adiposomes Promote Vascular Smooth Muscle Cell Hypercontractility.Comprehensive Physiology · 2025Article
- Endothelial TERT drives microvascular phenotype associated with coronary artery disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- Altered endothelial mitochondrial Opa1-related fusion in mouse accelerates age-associated vascular and kidney damage.Physiological reports · 2025Article
- A chronology of basic and clinical research in the coronary microcirculation.Journal of molecular and cellular cardiology · 2025Article
- Sexually dimorphic mechanisms of HJournal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Activity and function of the endothelial sodium channel is regulated by the effector domain of MARCKS-like protein 1 in mouse aortic endothelial cells.American journal of physiology. Cell physiology · 2025Article
36 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
rationaleMitochondrial-derived hydrogen peroxide (H2O2) regulates flow-induced dilation (FID) in microvessels from patients with coronary artery disease. The relationship between ceramide, an independent risk factor for coronary artery disease and a known inducer of mitochondrial reactive oxygen species, and FID is unknown.
objectiveWe examined the hypothesis that exogenous ceramide induces a switch in the mediator of FID from nitric oxide to H2O2. METHODS AND
resultsInternal diameter changes of resistance arterioles from human adipose and atrial tissue were measured by video microscopy. Mitochondrial H2O2 production was assayed in arterioles using mito peroxy yellow 1. Polyethylene glycol-catalase, rotenone, and Mito-TEMPO impaired FID in healthy adipose arterioles pretreated with ceramide, whereas N(ω)-nitro-l-arginine methyl ester had no effect. Mitochondrial H2O2 production was induced in response to flow in healthy adipose vessels pretreated with ceramide, and this was abolished in the presence of polyethylene glycol-catalase. Immunohistochemistry demonstrated ceramide accumulation in arterioles from both healthy patients and patients with coronary artery disease. N(ω)-nitro-l-arginine methyl ester reduced vasodilation to flow in adipose as well as atrial vessels from patients with coronary artery disease incubated with GW4869, a neutral sphingomyelinase inhibitor, whereas polyethylene glycol-catalase had no effect.
conclusionsOur data indicate that ceramide has an integral role in the transition of the mediator of FID from nitric oxide to mitochondrial-derived H2O2 and that inhibition of ceramide production can revert the mechanism of dilation back to nitric oxide. Ceramide may be an important target for preventing and treating vascular dysfunction associated with atherosclerosis.
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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.