ArticleScientific reports2016
NADPH oxidase 4 deficiency increases tubular cell death during acute ischemic reperfusion injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Alpha-1 Antitrypsin Protects Against Cisplatin-Induced Acute Kidney Injury by Restoring Redox and Mitochondrial Homeostasis.Biomolecules · 2026Article
- Therapeutic Potential of Apocynin: A Promising Antioxidant Strategy for Acute Kidney Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Mechanism of xanthine oxidase in flap ischemia-reperfusion injury and advances in targeted therapy: a mini review.Frontiers in physiology · 2025Review
- Acidic preconditioning induced intracellular acid adaptation to protect renal injury via dynamic phosphorylation of focal adhesion kinase-dependent activation of sodium hydrogen exchanger 1.Cell communication and signaling : CCS · 2024Article
- Specific NOX4 Inhibition Preserves Mitochondrial Function and Dampens Kidney Dysfunction Following Ischemia-Reperfusion-Induced Kidney Injury.Antioxidants (Basel, Switzerland) · 2024Article
- Neutrophils and NADPH Oxidases Are Major Contributors to Mild but Not Severe Ischemic Acute Kidney Injury in Mice.International journal of molecular sciences · 2024Article
- High resolution spatial profiling of kidney injury and repair using RNA hybridization-based in situ sequencing.Nature communications · 2024Article
- The regulation of cardiac intermediary metabolism by NADPH oxidases.Cardiovascular research · 2023Review
- NOX4 is a potential therapeutic target in septic acute kidney injury by inhibiting mitochondrial dysfunction and inflammation.Theranostics · 2023Article
- Impact ofIranian journal of biotechnology · 2022Article
- Novel role of macrophage TXNIP-mediated CYLD-NRF2-OASL1 axis in stress-induced liver inflammation and cell death.JHEP reports : innovation in hepatology · 2022Article
- Cathepsin K Deficiency Prevented Kidney Damage and Dysfunction in Response to 5/6 Nephrectomy Injury in Mice With or Without Chronic Stress.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Mechanism of kidney injury induced by cisplatin.Toxicology research · 2022Review
- NADPH-oxidase 4 gene over-expression in peripheral blood lymphocytes of the schizophrenia patients.PloS one · 2022Article
- Innovations and Emerging Therapies to Combat Renal Cell Damage: NADAntioxidants & redox signaling · 2021Review
- Genetic deletion of Nox4 enhances cancerogen-induced formation of solid tumors.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A Cell-Penetrating Peptide That Blocks Toll-Like Receptor Signaling Protects Kidneys against Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Article
- New insights into the role of heme oxygenase-1 in acute kidney injury.Kidney research and clinical practice · 2020Review
- NADPH oxidase 4 is protective and not fibrogenic in intestinal inflammation.Redox biology · 2020Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NADPH oxidase 4 (NOX4) is highly expressed in kidney proximal tubular cells. NOX4 constitutively produces hydrogen peroxide, which may regulate important pro-survival pathways. Renal ischemia reperfusion injury (IRI) is a classical model mimicking human ischemic acute tubular necrosis. We hypothesized that NOX4 plays a protective role in kidney IRI. In wild type (WT) animals subjected to IRI, NOX4 protein expression increased after 24 hours. NOX4 KO (knock-out) and WT littermates mice were subjected to IRI. NOX4 KO mice displayed decreased renal function and more severe tubular apoptosis, decreased Bcl-2 expression and higher histologic damage scores compared to WT. Activation of NRF2 was decreased in NOX4 KO mice in response to IRI. This was related to decreased KEAP1 oxidation leading to decreased NRF2 stabilization. This resulted in decreased glutathione levels. In vitro silencing of NOX4 in cells showed an enhanced propensity to apoptosis, with reduced expression of NRF2, glutathione content and Bcl-2 expression, similar to cells derived from NOX4 KO mice. Overexpression of a constitutively active form of NRF2 (caNRF2) in NOX4 depleted cells rescued most of this phenotype in cultured cells, implying that NRF2 regulation by ROS issued from NOX4 may play an important role in its anti-apoptotic property.
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