ArticleAntioxidants (Basel, Switzerland)2022
Selective Pharmacological Inhibition of NOX2 by GSK2795039 Improves Bladder Dysfunction in Cyclophosphamide-Induced Cystitis in Mice.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Triamcinolone acetonide nanoparticles ameliorate interstitial cystitis and anxiety/depression by targeting the bladder-metabolic-brain axis.Materials today. Bio · 2026Article
- Redox Imbalance and NOS-Dependent Modulation of Superoxide in the Bladder Mucosa of Women With IC/BPS: A Preliminary Study.Journal of cellular and molecular medicine · 2026Article
- Oxidative Stress, Environmental Pollutants, Aging, and Epigenetic Regulation: Mechanistic Insights and Biomarker Advances.Antioxidants (Basel, Switzerland) · 2026Review
- Strain-level heterogeneity in Gardnerella urinary tract persistence and pathogenesis in an in vivo model is consistent with comparative phylogenomic analyses.BMC microbiology · 2026Article
- Signaling pathways related to interstitial cystitis.Frontiers in immunology · 2026Review
- Piezo2 in sensory neurons contributes to inflammation-induced bladder overactivity and is associated with the effects of electroacupuncture.Frontiers in neuroscience · 2026Article
- Bladder Dysfunction in Sickle Cell Disease Is Associated with Inflammation and Oxidative Stress.International journal of molecular sciences · 2025Article
- Strain-level differences inbioRxiv : the preprint server for biology · 2025Article
- Pterostilbene Reduces Cyclophosphamide-Induced Interstitial Cystitis by Facilitating Nrf2 Activation and Suppressing the NLRP3 Inflammasome Pathway.International journal of molecular sciences · 2025Article
- ML-UrineQuant: A machine learning program for identifying and quantifying mouse urine on absorbent paper.Physiological reports · 2025Article
- Oxidative stress mediated by the NOX2/ROS/NF-κB signaling axis is involved in rosacea.Archives of dermatological research · 2025Article
- NRF2 Deficiency in Bladder Epithelial Cells Owing to Ubiquitination by N6-Methyladenosine-Modified TRIM21 Induces Oxidative Stress and Inflammation to Aggravate IC/BPS.Journal of inflammation research · 2025Article
- Delineating the NOX-Mediated Promising Therapeutic Strategies for the Management of Various Cardiovascular Disorders: A Comprehensive Review.Current vascular pharmacology · 2025Review
- Targeting NADPH Oxidase as an Approach for Diabetic Bladder Dysfunction.Antioxidants (Basel, Switzerland) · 2024Review
- Methylglyoxal and Advanced Glycation End Products (AGEs): Targets for the Prevention and Treatment of Diabetes-Associated Bladder Dysfunction?Biomedicines · 2024Review
- SARS-CoV-2 Spike Protein Stimulates Macropinocytosis in Murine and Human Macrophages via PKC-NADPH Oxidase Signaling.Antioxidants (Basel, Switzerland) · 2024Article
- Impact of intravascular hemolysis on functional and molecular alterations in the urinary bladder: implications for an overactive bladder in sickle cell disease.Frontiers in physiology · 2024Article
- A Spectrum of Age- and Gender-Dependent Lower Urinary Tract Phenotypes in Three Mouse Models of Type 2 Diabetes.Metabolites · 2023Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory disease without consistently effective treatment. Among the many mediators implicated in cystitis, the overproduction of reactive oxygen species (ROS) seems to play a key role, although the main source of ROS remains unclear. This study aimed to investigate the contribution of NADPH oxidase (NOX) isoforms in ROS generation and the voiding dysfunction of cyclophosphamide (CYP, 300 mg/Kg, ip, 24 h)-induced cystitis in adult female mice, a well-recognized animal model to study IC/BPS, by using GKT137831 (5 mg/Kg, ip, three times in a 24 h period) or GSK2795039 (5 mg/Kg, ip, three times in a 24 h period) to inhibit NOX1/4 or NOX2, respectively. Our results showed that treatment with GSK2795039 improved the dysfunctional voiding behavior induced by CYP, reduced bladder edema and inflammation, and preserved the urothelial barrier integrity and tight junction occludin expression, besides inhibiting the characteristic vesical pain and bladder superoxide anion generation. In contrast, the NOX1/4 inhibitor GKT137831 had no significant protective effects. Taken together, our in vivo and ex vivo data demonstrate that NOX2 is possibly the main source of ROS observed in cystitis-induced CYP in mice. Therefore, selective inhibition of NOX2 by GSK2795039 may be a promising target for future therapies for IC/BPS.
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