ArticleCell death & disease2012
Molecular targeting of NOX4 for neuropathic pain after traumatic injury of the spinal cord.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.
- The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.Journal of clinical laboratory analysis · 2022Pooled it
- Identification and validation of MicroRNA-mRNA Networks in Dorsal Root Ganglia after Peripheral Nerve Injury.International journal of medical sciences · 2022Pooled it
- Association ofRadiology and oncology · 2023Trial
- Alteration of microRNA Expression Associated with Chronic Back Pain in Patients with Intervertebral Disc Degeneration: A Scoping Review.International journal of molecular sciences · 2026Article
- Identification of a reactive astrocyte subpopulation during HIV-associated pain pathogenesis in mouse models.Nature communications · 2025Article
- Exploration of Hub Genes and Immune Cell Infiltration Characteristics Associated With Spinal Cord Injury in Mice.Journal of inflammation research · 2025Article
- Advancements in Antioxidant-Based Therapeutics for Spinal Cord Injury: A Critical Review of Strategies and Combination Approaches.Antioxidants (Basel, Switzerland) · 2024Review
- Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.Current neuropharmacology · 2024Review
- Antisense oligodeoxynucleotides against dynamin-related protein 1 reduce remifentanil-induced hyperalgesia by modulating spinal N-methyl-D-aspartate receptor expression in rats.The Korean journal of pain · 2023Article
- Classifying Integrated Signature Molecules in Macrophages of Rheumatoid Arthritis, Osteoarthritis, and Periodontal Disease: An Omics-Based Study.Current issues in molecular biology · 2022Article
- Article
- Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021Review
- New Vistas in microRNA Regulatory Interactome in Neuropathic Pain.Frontiers in pharmacology · 2021Review
- Advances With Non-coding RNAs in Neuropathic Pain.Frontiers in neuroscience · 2021Review
- MicroRNA-330 Directs Downregulation of the GABAJournal of molecular neuroscience : MN · 2020Article
- Nociceptive related microRNAs and their role in rheumatoid arthritis.Molecular biology reports · 2020Review
- Non-coding RNAs in neuropathic pain.Neuronal signaling · 2020Review
- Down-Regulation of NOX4 Expression in Dorsal Horn of Spinal Cord Could Alleviate Cancer-Induced Bone Pain in Rats by Reducing Oxidative Stress Response.Cancer management and research · 2020Article
- Engagement of MicroRNA-155 in Exaggerated Oxidative Stress Signal and TRPA1 in the Dorsal Horn of the Spinal Cord and Neuropathic Pain During Chemotherapeutic Oxaliplatin.Neurotoxicity research · 2019Article
- Inhibition of NOX2 signaling limits pain-related behavior and improves motor function in male mice after spinal cord injury: Participation of IL-10/miR-155 pathways.Brain, behavior, and immunity · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is a well-known type of chronic pain caused by damage to the nervous system. Until recently, many researchers have primarily focused on identifying cellular or chemical sources of neuropathic pain or have approached neuropathic pain via the basis of biological study. We investigated whether both mmu-mir-23b (miR23b) and NADPH oxidase 4 (NOX4) antibody infusion can alleviate neuropathic pain by compensating for abnormally downregulated miR23b via reducing the expression of its target gene, NOX4, a reactive oxygen species (ROS) family member overexpressed in neuropathic pain. Ectopic miR23b expression effectively downregulated NOX4 and finally normalized glutamic acid decarboxylase 65/67 expression. Moreover, animals with neuropathic pain showed significantly improved paw withdrawal thresholds (PWTs) following miR23b infusion. Normalizing miR23b expression in tissue lesions, caused by neuropathic pain induction, reduced inflammatory mediators and increased several ROS scavengers. Moreover, γ-aminobutyric acid (GABA)ergic neurons coexpressed suboptimal levels of miR23b and elevated NOX4/ROS after pain induction at the cellular level. MiR23b finally protects GABAergic neurons against ROS/p38/c-Jun N-terminal kinase (JNK)-mediated apoptotic death. By evaluating the functional behavior of mice receiving pain/miR23b, normal/anti-miR23b, anti-miR23b/si-NOX4, pain/NOX4 antibody, pain/ascorbic acid, and pain/ascorbic acid/NOX4 antibody, the positive role of miR23b and the negative role of NOX4 in neuropathic pain were confirmed. Based on this study, we conclude that miR23b has a crucial role in the amelioration of neuropathic pain in injured spinal cord by inactivating its target gene, NOX4, and protection of GABAergic neurons from cell death. We finally suggest that infusion of miR23b and NOX4 antibody may provide attractive diagnostic and therapeutic resources for effective pain modulation in neuropathic pain.
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