ArticleRedox biology2014
Unique role of NADPH oxidase 5 in oxidative stress in human renal proximal tubule cells.
Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- Pan-Nox inhibitor treatment improves renal function in aging murine diabetic kidneys.Kidney research and clinical practice · 2024Article
- Endothelial NOX5 Obliterates the Reno-Protective Effect of Nox4 Deletion by Promoting Renal Fibrosis via Activation of EMT and ROS-Sensitive Pathways in Diabetes.Antioxidants (Basel, Switzerland) · 2024Article
- NADPH oxidase inhibitor development for diabetic nephropathy through water tank model.Kidney research and clinical practice · 2022Article
- Central role of c-Src in NOX5- mediated redox signalling in vascular smooth muscle cells in human hypertension.Cardiovascular research · 2022Article
- Renal Dopamine Receptors and Oxidative Stress: Role in Hypertension.Antioxidants & redox signaling · 2021Review
- Coordinated Contribution of NADPH Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Metabolic Syndrome and Its Implication in Renal Dysfunction.Frontiers in pharmacology · 2021Review
- NOX Inhibitors: From Bench to Naxibs to Bedside.Handbook of experimental pharmacology · 2021Article
- NOX5-induced uncoupling of endothelial NO synthase is a causal mechanism and theragnostic target of an age-related hypertension endotype.PLoS biology · 2020Article
- Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Review
- Inhibition of NADPH Oxidase 5 (NOX5) Suppresses High Glucose-Induced Oxidative Stress, Inflammation and Extracellular Matrix Accumulation in Human Glomerular Mesangial Cells.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Function of NADPH Oxidases in Diabetic Nephropathy and Development of Nox Inhibitors.Biomolecules & therapeutics · 2020Review
- Genetic polymorphisms associated with reactive oxygen species and blood pressure regulation.The pharmacogenomics journal · 2019Review
- Vascular Biology of Superoxide-Generating NADPH Oxidase 5-Implications in Hypertension and Cardiovascular Disease.Antioxidants & redox signaling · 2019Review
- NDRG2 contributes to cisplatin sensitivity through modulation of BAK-to-Mcl-1 ratio.Cell death & disease · 2018Article
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
NADPH oxidases are the major sources of reactive oxygen species in cardiovascular, neural, and kidney cells. The NADPH oxidase 5 (NOX5) gene is present in humans but not rodents. Because Nox isoforms in renal proximal tubules (RPTs) are involved in the pathogenesis of hypertension, we tested the hypothesis that NOX5 is differentially expressed in RPT cells from normotensive (NT) and hypertensive subjects (HT). We found that NOX5 mRNA, total NOX5 protein, and apical membrane NOX5 protein were 4.2±0.7-fold, 5.2±0.7-fold, and 2.8±0.5-fold greater in HT than NT. Basal total NADPH oxidase activity was 4.5±0.2-fold and basal NOX5 activity in NOX5 immunoprecipitates was 6.2±0.2-fold greater in HT than NT (P=<0.001, n=6-14/group). Ionomycin increased total NOX and NOX5 activities in RPT cells from HT (P<0.01, n=4, ANOVA), effects that were abrogated by pre-treatment of the RPT cells with diphenylene-iodonium or superoxide dismutase. Silencing NOX5 using NOX5-siRNA decreased NADPH oxidase activity (-45.1±3.2% vs. mock-siRNA, n=6-8) in HT. D1-like receptor stimulation decreased NADPH oxidase activity to a greater extent in NT (-32.5±1.8%) than HT (-14.8±1.8). In contrast to the marked increase in expression and activity of NOX5 in HT, NOX1 mRNA and protein were minimally increased in HT, relative to NT; total NOX2 and NOX4 proteins were not different between HT and NT, while the increase in apical RPT cell membrane NOX1, NOX2, and NOX4 proteins in HT, relative to NT, was much less than those observed with NOX5. Thus, we demonstrate, for the first time, that NOX5 is expressed in human RPT cells and to greater extent than the other Nox isoforms in HT than NT. We suggest that the increased expression of NOX5, which may be responsible for the increased oxidative stress in RPT cells in human essential hypertension, is caused, in part, by a defective renal dopaminergic system.
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Registered trials
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