ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Endothelial Nox4-based NADPH oxidase regulates atherosclerosis via soluble epoxide hydrolase.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Dual therapy with vildagliptin and sacubitril/valsartan alleviates portal hypertension and inhibits soluble epoxide hydrolase in cirrhotic rats.World journal of gastroenterology · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Searching for Hub Genes of Quince-Basil Co-Administration Against Atherosclerosis Using Bioinformatics Analysis and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Mitochondrial dysfunction and metabolic reprogramming induce macrophage pro-inflammatory phenotype switch and atherosclerosis progression in aging.Frontiers in immunology · 2024Article
- The involvement of soluble epoxide hydrolase in the development of cardiovascular diseases through epoxyeicosatrienoic acids.Frontiers in pharmacology · 2024Review
- Studies on the Effects of Hypercholesterolemia on Mouse Ophthalmic Artery Reactivity.Diseases (Basel, Switzerland) · 2023Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- CYP450 Epoxygenase Metabolites, Epoxyeicosatrienoic Acids, as Novel Anti-Inflammatory Mediators.Molecules (Basel, Switzerland) · 2022Review
- Oxidative Injury in Ischemic Stroke: A Focus on NADPH Oxidase 4.Oxidative medicine and cellular longevity · 2022Review
- NF-κB and its crosstalk with endoplasmic reticulum stress in atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Endothelial dysfunction due to the inhibition of the synthesis of nitric oxide: Proposal and characterization of anFrontiers in physiology · 2022Article
- Article
- Mechanisms of Endothelial Dysfunction in Pre-eclampsia and Gestational Diabetes Mellitus: Windows Into Future Cardiometabolic Health?Frontiers in endocrinology · 2020Review
- The Role of NADPH Oxidases in the Etiology of Obesity and Metabolic Syndrome: Contribution of Individual Isoforms and Cell Biology.Antioxidants & redox signaling · 2019Review
- NADPH Oxidase 4 Regulates Inflammation in Ischemic Heart Failure: Role of Soluble Epoxide Hydrolase.Antioxidants & redox signaling · 2019Article
- MicroRNA-30e regulates TGF-β-mediated NADPH oxidase 4-dependent oxidative stress by Snai1 in atherosclerosis.International journal of molecular medicine · 2019Article
- NADPH oxidase 4 and its role in the cardiovascular system.Vascular biology (Bristol, England) · 2019Review
- Myocardial Ischemia and Diabetes Mellitus: Role of Oxidative Stress in the Connection between Cardiac Metabolism and Coronary Blood Flow.Journal of diabetes research · 2019Review
- ROS signaling and ER stress in cardiovascular disease.Molecular aspects of medicine · 2018Review
- Reactive Oxygen Species in Metabolic and Inflammatory Signaling.Circulation research · 2018Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Nox4-based NADPH oxidase is a major reactive oxygen species-generating enzyme in the vasculature, but its role in atherosclerosis remains controversial.
objectiveOur goal was to investigate the mechanisms of endothelial Nox4 in regulating atherosclerosis. APPROACH AND
resultsAtherosclerosis-prone conditions (disturbed blood flow, type I diabetes, and Western diet) downregulated endothelial Nox4 mRNA in arteries. To address whether the downregulated endothelial Nox4 was directly involved in the development of atherosclerosis, we generated mice carrying a human Nox4 P437H dominant negative mutation (Nox4DN), driven by the endothelial specific promoter Tie-2, on atherosclerosis-prone genetic background (ApoE deficient mice) to mimic the effect of decreased endothelial Nox4. Nox4DN significantly increased type I diabetes-induced aortic stiffness and atherosclerotic lesions. Gene analysis indicated that soluble epoxide hydrolase 2 (sEH) was significantly upregulated in Nox4DN endothelial cells (EC). Inhibition of sEH activity in Nox4DN EC suppressed inflammation and macrophage adhesion to EC. On the contrary, overexpression of endothelial wild type Nox4 suppressed sEH, ameliorated Western diet-induced atherosclerosis and decreased aortic stiffness.
conclusionsAtherosclerosis-prone conditions downregulated endothelial Nox4 to accelerate the progress of atherosclerosis, at least in part, by upregulating sEH to enhance inflammation.
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