ArticleFrontiers in immunology2023
Mitochondrial ROS and base excision repair steps leading to DNA nick formation drive ultraviolet induced-NETosis.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Neutrophil Extracellular Traps in Viral Infections.Pathogens (Basel, Switzerland) · 2025Pooled it
- A high-throughput, plate reader-based method for the assessment of oxidative stress in suspension mammalian cells using CellROX Green.Histochemistry and cell biology · 2026Article
- Redox-modulation of regulated cell death: implications for synergistic anticancer therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis.Redox biology · 2026Article
- Mitochondria-targeted nanozyme system for psoriasis treatment.Journal of nanobiotechnology · 2026Article
- Neutrophil extracellular traps in gout: from immune defense to pathological dynamic equilibrium.Frontiers in immunology · 2026Review
- Panoramic description of ROS-based nanotechnology for osteomyelitis therapy: Challenges, opportunities, and prospects.Theranostics · 2026Review
- Advances in gene therapy for mitochondrial genetic disorders: current status and clinical implementation challenges.Journal of translational medicine · 2025Review
- The role of epigenetic regulation in cuproptosis, ferroptosis and NETosis in the pathogenesis of autoimmune diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Review
- Neutrophil extracellular traps and metabolic reprogramming in renal cell carcinoma: implications for tumor progression and immune-based therapeutics.Cancer biology & medicine · 2025Review
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Antioxidants as Modulators of NETosis: Mechanisms, Evidence, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Mitochondrial Transplantation/Transfer: Promising Therapeutic Strategies for Spinal Cord Injury.Journal of orthopaedic translation · 2025Review
- Ischemia-reperfusion injury after spinal cord decompressive surgery-An in vivo rat model.Animal models and experimental medicine · 2025Article
- N-benzyl-N-methyldecane-1-amine derived from garlic ameliorates UVB-induced photoaging in HaCaT cells and SKH-1 hairless mice.Scientific reports · 2025Article
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- Cyclic stretch enhances neutrophil extracellular trap formation.BMC biology · 2024Article
- A metabolic perspective of the neutrophil life cycle: new avenues in immunometabolism.Frontiers in immunology · 2023Review
- Human HLA prolongs the host inflammatory response inFrontiers in cellular and infection microbiology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) is essential for neutrophil extracellular trap formation (NETosis), and generated either by NADPH oxidases (e.g., during infections) or mitochondria (e.g., sterile injury) in neutrophils. We recently showed that ultraviolet (UV) radiation, a sterile injury-inducing agent, dose-dependently induced mitochondrial ROS generation, and increasing levels of ROS shifted the neutrophil death from apoptosis to NETosis. Nevertheless, how ROS executes UV-induced NETosis is unknown. In this study, we first confirmed that UV doses used in our experiments generated mitochondrial ROS, and the inhibition of mitochondrial ROS suppressed NETosis (Mitosox, SYTOX, immunocytochemistry, imaging). Next, we showed that UV irradiation extensively oxidized DNA, by confocal imaging of 8-oxyguanine (8-oxoG) in NETs. Immunofluorescence microscopy further showed that a DNA repair protein, proliferating cell nuclear antigen, was widely distributed throughout the DNA, indicating that the DNA repair machinery was active throughout the genome during UV-induced NETosis. Inhibition of specific steps of base excision repair (BER) pathway showed that steps leading up to DNA nick formation, but not the later steps, suppressed UV-induced NETosis. In summary, this study shows that (i) high levels of mitochondrial ROS produced following UV irradiation induces extensive oxidative DNA damage, and (ii) early steps of the BER pathway leading to DNA nicking results in chromatin decondensation and NETosis. Collectively, these findings reveal how ROS induces NOX-independent NETosis, and also a novel biological mechanism for UV irradiation- and -mitochondrial ROS-mediated NETosis.
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