ArticleJournal of the American Society of Nephrology : JASN2014
Nephropathy and elevated BP in mice with podocyte-specific NADPH oxidase 5 expression.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 126 citations in OpenAlex.
- Synergistic Network Pharmacology: Preclinical Validation and Clinical Safety in Acute Ischemic Stroke.Journal of the American Heart Association · 2025Trial
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- F-actin-dependent activation of NADPH oxidase 5 by the vacuolar-type ATPase.The Journal of biological chemistry · 2026Article
- Interactions between Tau Phosphorylation and Endoplasmic Reticulum Stress in Diabetic Nephropathy.Diabetes & metabolism journal · 2026Article
- Mitophagy and oxidative stress in chronic kidney disease (Review).Molecular medicine reports · 2026Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.Journal of the American Society of Nephrology : JASN · 2025Review
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Association Between GGT/HDL-C Ratio and Diabetic Kidney Disease in Patients with Type-2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- The Role of Oxidative Stress in Hypertension: The Insight into Antihypertensive Properties of Vitamins A, C and E.Antioxidants (Basel, Switzerland) · 2024Review
- Diabetes and Renal Complications: An Overview on Pathophysiology, Biomarkers and Therapeutic Interventions.Biomedicines · 2024Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- 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
- Associations between non-insulin-based insulin resistance indices and diabetic nephropathy in patients with diabetes mellitus in US adults: a cross-sectional study of NHANES 1999-2018.Frontiers in endocrinology · 2024Article
- The Role of Oxidative Stress in Kidney Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Redox regulation in diabetic kidney disease.American journal of physiology. Renal physiology · 2023Review
- Structure, regulation, and physiological functions of NADPH oxidase 5 (NOX5).Journal of physiology and biochemistry · 2023Review
- Molecular Genetics of Abnormal Redox Homeostasis in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Functional interactions between NADPH oxidase 5 and actin.Frontiers in cell and developmental biology · 2023Article
- Endothelial reactive oxygen-forming NADPH oxidase 5 is a possible player in diabetic aortic aneurysm but not atherosclerosis.Scientific reports · 2022Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
NADPH oxidase (Nox) enzymes are a significant source of reactive oxygen species, which contribute to glomerular podocyte dysfunction. Although studies have implicated Nox1, -2, and -4 in several glomerulopathies, including diabetic nephropathy, little is known regarding the role of Nox5 in this context. We examined Nox5 expression and regulation in kidney biopsies from diabetic patients, cultured human podocytes, and a novel mouse model. Nox5 expression increased in human diabetic glomeruli compared with nondiabetic glomeruli. Stimulation with angiotensin II upregulated Nox5 expression in human podocyte cultures and increased reactive oxygen species generation. siRNA-mediated Nox5 knockdown inhibited angiotensin II-stimulated production of reactive oxygen species and altered podocyte cytoskeletal dynamics, resulting in an Rac-mediated motile phenotype. Because the Nox5 gene is absent in rodents, we generated transgenic mice expressing human Nox5 in a podocyte-specific manner (Nox5(pod+)). Nox5(pod+) mice exhibited early onset albuminuria, podocyte foot process effacement, and elevated systolic BP. Subjecting Nox5(pod+) mice to streptozotocin-induced diabetes further exacerbated these changes. Our data show that renal Nox5 is upregulated in human diabetic nephropathy and may alter filtration barrier function and systolic BP through the production of reactive oxygen species. These findings provide the first evidence that podocyte Nox5 has an important role in impaired renal function and hypertension.
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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.