ArticleScientific reports2016
Apocynin and Nox2 regulate NF-κB by modifying thioredoxin-1 redox-state.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
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- NOX2 deficiency exacerbates lupus nephritis through activation of NLRP3 inflammasome in neutrophils.Journal of biomedical science · 2026Article
- A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension.Redox biology · 2026Article
- Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026Review
- Extracellular Redox Balance as a Determinant of Immune Regulation and Tissue Inflammation.Antioxidants (Basel, Switzerland) · 2026Review
- Reductive stress in cancer immunology and targeted therapy.Acta biochimica et biophysica Sinica · 2026Review
- The novel thioredoxin reductase inhibitor butaselen suppresses lung cancer by inducing oxidative stress.Redox report : communications in free radical research · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Oxidative stress mediated by the NOX2/ROS/NF-κB signaling axis is involved in rosacea.Archives of dermatological research · 2025Article
- NADPCurrent medicinal chemistry · 2025Review
- MnTheranostics · 2025Article
- Protective effect of zerumbone on sepsis-induced acute lung injury through anti-inflammatory and antioxidative activity via NF-κB pathway inhibition and HO-1 activation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- TNFα: TNFR1 signaling inhibits maturation and maintains the pro-inflammatory programming of monocyte-derived macrophages in murine chronic granulomatous disease.Frontiers in immunology · 2024Article
- NADPH oxidase 2 limits amplification of IL-1β-G-CSF axis and an immature neutrophil subset in murine lung inflammation.Blood advances · 2023Article
- Neutrophil-Derived Tumor Necrosis Factor Drives Fungal Acute Lung Injury in Chronic Granulomatous Disease.The Journal of infectious diseases · 2021Article
- Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021Review
- Novel and Converging Ways of NOX2 and SOD3 in Trafficking and Redox Signaling in Macrophages.Antioxidants (Basel, Switzerland) · 2021Review
- From Flies to Men: ROS and the NADPH Oxidase in Phagocytes.Frontiers in cell and developmental biology · 2021Review
- Reactive Oxygen Species: Not Omnipresent but Important in Many Locations.Frontiers in cell and developmental biology · 2021Article
- MnTE-2-PyP, a manganese porphyrin, reduces cytotoxicity caused by irradiation in a diabetic environment through the induction of endogenous antioxidant defenses.Redox biology · 2020Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
Abstract
The reactive-oxygen-species-(ROS)-generating-enzyme Nox2 is essential for leukocyte anti-microbial activity. However its role in cellular redox homeostasis and, consequently, in modulating intracellular signaling pathways remains unclear. Herein, we show Nox2 activation favors thioredoxin-1 (TRX-1)/p40phox interaction, which leads to exclusion of TRX-1 from the nucleus. In contrast, the genetic deficiency of Nox2 or its pharmacological inhibition with apocynin (APO) results in reductive stress after lipopolysaccharide-(LPS)-cell stimulation, which causes nuclear accumulation of TRX-1 and enhanced transcription of inflammatory mediators through nuclear-factor-(NF)-κB. The NF-κB overactivation is prevented by TRX-1 oxidation using inhibitors of thioredoxin reductase-1 (TrxR-1). The Nox2/TRX-1/NF-κB intracellular signaling pathway is involved in the pathophysiology of chronic granulomatous disease (CGD) and sepsis. In fact, TrxR-1 inhibition prevents nuclear accumulation of TRX-1 and LPS-stimulated hyperproduction of tumor-necrosis-factor-(TNF)-α by monocytes and neutrophils purified from blood of CGD patients, who have deficient Nox2 activity. TrxR-1 inhibitors, either lanthanum chloride (LaCl
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