ArticlePloS one2018
Oxidative stress caused by activation of NADPH oxidase 4 promotes contrast-induced acute kidney injury.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 69 citations in OpenAlex.
- Combined Apocynin and Novokinin Treatment Attenuates Renal Damage and Reduces KIM-1 Expression in a Model of Ischemic AKI.International journal of molecular sciences · 2026Article
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.Aging cell · 2026Article
- The MICOS Complex Regulates Mitochondrial Structure and Oxidative Stress During Age-Dependent Structural Deficits in the Kidney.bioRxiv : the preprint server for biology · 2026Article
- Cetirizine ameliorates cyclophosphamide-induced placental toxicity via modulation of TGF-β/NOX4 signaling pathway in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Integration of network pharmacology and transcriptomics to reveal the ROS/NLRP3/Caspase-1/GSDMD-mediated mechanism of baicalin in alleviating contrast-induced acute kidney injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Vitamin E for the Prevention of Contrast-Induced Nephropathy: A Systematic Review and Meta-Analysis.Cureus · 2024Review
- The intellectual base and global trends in contrast-induced acute kidney injury: a bibliometric analysis.Renal failure · 2023Article
- The Potential Biotherapeutic Targets of Contrast-Induced Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Taurine as Antioxidant in a Novel Cell- and Oxygen Carrier-Free Perfusate for Normothermic Machine Perfusion of Porcine Kidneys.Antioxidants (Basel, Switzerland) · 2023Article
- Hypoxia-Induced Kidney Injury in Newborn Rats.Toxics · 2023Article
- Mineralocorticoid Receptor Antagonism Attenuates Multiple Organ Failure after Renal Ischemia and Reperfusion in Mice.International journal of molecular sciences · 2023Article
- Pre-clinical evidence of a dual NADPH oxidase 1/4 inhibitor (setanaxib) in liver, kidney and lung fibrosis.Journal of cellular and molecular medicine · 2023Review
- NOX4 is a potential therapeutic target in septic acute kidney injury by inhibiting mitochondrial dysfunction and inflammation.Theranostics · 2023Article
- NADPH oxidase 4 inhibition is a complementary therapeutic strategy for spinal muscular atrophy.Frontiers in cellular neuroscience · 2023Article
- Selective Pharmacological Inhibition of NOX2 by GSK2795039 Improves Bladder Dysfunction in Cyclophosphamide-Induced Cystitis in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Ameliorative Effects of a Rhenium (V) Compound with Uracil-Derived Ligand Markers Associated with Hyperglycaemia-Induced Renal Dysfunction in Diet-Induced Prediabetic Rats.International journal of molecular sciences · 2022Article
- Carnosine Alleviates Knee Osteoarthritis and Promotes Synoviocyte Protection via Activating the Nrf2/HO-1 Signaling Pathway: An In-Vivo and In-Vitro Study.Antioxidants (Basel, Switzerland) · 2022Article
- NADPH oxidase family proteins: signaling dynamics to disease management.Cellular & molecular immunology · 2022Review
- Simultaneous stabilization of actin cytoskeleton in multiple nephron-specific cells protects the kidney from diverse injury.Nature communications · 2022Article
- Ceria-Zirconia nanoparticles reduce intracellular globotriaosylceramide accumulation and attenuate kidney injury by enhancing the autophagy flux in cellular and animal models of Fabry disease.Journal of nanobiotechnology · 2022Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contrast-induced acute kidney injury (CIAKI) is a leading cause of acute kidney injury following radiographic procedures. Intrarenal oxidative stress plays a critical role in CIAKI. Nicotinamide adenine dinucleotide 3-phosphate (NADPH) oxidases (Noxs) are important sources of reactive oxygen species (ROS). Among the various types of Noxs, Nox4 is expressed predominantly in the kidney in rodents. Here, we evaluated the role of Nox4 and benefit of Nox4 inhibition on CIAKI using in vivo and in vitro models. HK-2 cells were treated with iohexol, with or without Nox4 knockdown, or the most specific Nox1/4 inhibitor (GKT137831). Effects of Nox4 inhibition on CIAKI mice were examined. Expression of Nox4 in HK-2 cells was significantly increased following iohexol exposure. Silencing of Nox4 rescued the production of ROS, downregulated pro-inflammatory markers (particularly phospho-p38) implicated in CIAKI, and reduced Bax and caspase 3/7 activity, which resulted in increased cellular survival in iohexol-treated HK-2 cells. Pretreatment with GKT137831 replicated these effects by decreasing levels of phospho-p38. In a CIAKI mouse model, even though the improvement of plasma blood urea nitrogen was unclear, pretreatment with GKT137831 resulted in preserved structure, reduced expression of 8-hydroxy-2'-deoxyguanosine (8OHdG) and kidney injury molecule-1 (KIM-1), and reduced number of TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling)-positive cells. These results suggest Nox4 as a key source of reactive oxygen species responsible for CIAKI and provide a novel potential option for prevention of CIAKI.
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