ArticleJournal of neuroinflammation2021
Oxidative stress induced by NOX2 contributes to neuropathic pain via plasma membrane translocation of PKCε in rat dorsal root ganglion neurons.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- PARP1 rewires neuroinflammatory and redox metabolism associated with reactive neuroglia in neuropathic pain.Redox biology · 2026Article
- Elevated 18:1 lysophosphatidylcholine contributes to neuropathic pain in peripheral nerve injury.Regional anesthesia and pain medicine · 2026Article
- A spinal USP7-Bach1 positive feedback loop drives NOX4-mediated ferroptosis in neuropathic pain.Redox biology · 2026Article
- Article
- Mechanistic Insights into Antioxidant Interventions Targeting Obesity-Induced Oxidative Stress in the Pathogenesis and Complications of Type 2 Diabetes Mellitus.Current issues in molecular biology · 2025Review
- Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.Redox report : communications in free radical research · 2025Article
- NOX2 Contributes to High-Frequency Outer Hair Cell Vulnerability in the Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Botulinum toxin type A inhibits microglia pyroptosis by suppressing Cblb-mediated degradation of Pdlim1 to attenuate neuropathic pain.The journal of headache and pain · 2025Article
- Translating Basic Science to Clinical Applications: A Narrative Review of Repurposed Pharmacological Agents in Preclinical Models of Diabetic Neuropathy.Biomedicines · 2025Review
- Neuroprotectin D1 and GPR37 protect against chemotherapy-induced peripheral neuropathy and the transition from acute to chronic pain.Pharmacological research · 2025Article
- Effects and Mechanisms of Paeoniflorin in Relieving Neuropathic Pain: Network Pharmacological Analysis and Experimental Validation.Neurochemical research · 2025Article
- Mesenchymal stem cells as a therapeutic strategy to combat oxidative stress-mediated neuropathic pain.BioImpacts : BI · 2025Review
- Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this mapReview
- DNA damage induced PARP-1 overactivation confers paclitaxel-induced neuropathic pain by regulating mitochondrial oxidative metabolism.CNS neuroscience & therapeutics · 2024Article
- Role of EPAC1 in chronic pain.Biochemistry and biophysics reports · 2024Review
- Reactive Oxygen Species Induced Upregulation of TRPV1 in Dorsal Root Ganglia Results in Low Back Pain in Rats.Journal of inflammation research · 2024Article
- New perspectives in diabetic neuropathy.Neuron · 2023Review
- Activation of neuronal NADPH oxidase NOX2 promotes inflammatory neurodegeneration.Free radical biology & medicine · 2023Article
- Antinociceptive Effects of Aaptamine, a Sponge Component, on Peripheral Neuropathy in Rats.Marine drugs · 2023Article
- Effects of NADPH Oxidase Isoform-2 (NOX2) Inhibition on Behavioral Responses and Neuroinflammation in a Mouse Model of Neuropathic Pain.Biomedicines · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundNicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2)-induced oxidative stress, including the production of reactive oxygen species (ROS) and hydrogen peroxide, plays a pivotal role in neuropathic pain. Although the activation and plasma membrane translocation of protein kinase C (PKC) isoforms in dorsal root ganglion (DRG) neurons have been implicated in multiple pain models, the interactions between NOX2-induced oxidative stress and PKC remain unknown.
methodsA spared nerve injury (SNI) model was established in adult male rats. Pharmacologic intervention and AAV-shRNA were applied locally to DRGs. Pain behavior was evaluated by Von Frey tests. Western blotting and immunohistochemistry were performed to examine the underlying mechanisms. The excitability of DRG neurons was recorded by whole-cell patch clamping.
resultsSNI induced persistent NOX2 upregulation in DRGs for up to 2 weeks and increased the excitability of DRG neurons, and these effects were suppressed by local application of gp91-tat (a NOX2-blocking peptide) or NOX2-shRNA to DRGs. Of note, the SNI-induced upregulated expression of PKCε but not PKC was decreased by gp91-tat in DRGs. Mechanical allodynia and DRG excitability were increased by ψεRACK (a PKCε activator) and reduced by εV1-2 (a PKCε-specific inhibitor). Importantly, εV1-2 failed to inhibit SNI-induced NOX2 upregulation. Moreover, the SNI-induced increase in PKCε protein expression in both the plasma membrane and cytosol in DRGs was attenuated by gp91-tat pretreatment, and the enhanced translocation of PKCε was recapitulated by H
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