ArticleMolecular neurobiology2021
NGF-Induced Nav1.7 Upregulation Contributes to Chronic Post-surgical Pain by Activating SGK1-Dependent Nedd4-2 Phosphorylation.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of liposomal bupivacaine parasternal block combined with rectus sheath block on postoperative pain in patients undergoing sternotomy for cardiac surgery: a randomized controlled trial.BMC anesthesiology · 2026Trial
- The Therapeutic Role of Dienogest in Endometriosis-Associated Pain: From Basics to Clinics.Biomolecules · 2026Review
- From the Pain Matrix to Functional Networks: A Narrative Review of Chronic Pain Mechanisms Across Adult and Pediatric Populations with Emerging AI Perspectives.Brain sciences · 2026Review
- Fibromyalgia: A Multifactorial Pain Disorder.International journal of molecular sciences · 2026Review
- NaThe Journal of comparative neurology · 2026Article
- Palmitic acid aggravates atopic dermatitis by regulating SGK1/NEDD4L-involved cutaneous neuroimmune inflammation through driving TRPV1 and MRGPRB2 S-palmitoylation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Beyond Osteoarthritis: Emerging Applications of Anti-NGF Monoclonal Antibodies in Pain Management in Dogs and Cats.Animals : an open access journal from MDPI · 2025Review
- Unidirectional Crosstalk Between NTRK1 and IGF2 Drives ER Stress in Chronic Pain.Biomedicines · 2025Article
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Chronic Post-Surgical Pain After Hip and Knee Arthroplasty: An Update on Mechanisms, Risk Factors, and Interventional Treatment Modalities.Journal of pain research · 2025Review
- Decoding pain chronification: mechanisms of the acute-to-chronic transition.Frontiers in molecular neuroscience · 2025Review
- The role of SGK1 in neurologic diseases: A friend or foe?IBRO neuroscience reports · 2024Review
- Vitamin DCNS neuroscience & therapeutics · 2024Article
- Schwann cell-secreted PGECell · 2024Article
- 1953-2023. Seventy Years of the Nerve Growth Factor: A Potential Novel Treatment in Neurological Diseases?Aging and disease · 2024Review
- Histone deacetylase as emerging pharmacological therapeutic target for neuropathic pain: From epigenetic to selective drugs.CNS neuroscience & therapeutics · 2024Review
- Standardized Centella asiatica extract ECa 233 alleviates pain hypersensitivity by modulating P2X3 in trigeminal neuropathic pain.Journal of applied oral science : revista FOB · 2024Article
- Suberoylanilide Hydroxamic Acid Ameliorates Pain Sensitization in Central Neuropathic Pain After Spinal Cord Injury via the HDAC5/NEDD4/SCN9A Axis.Neurochemical research · 2023Article
- Integrative miRNA-mRNA profiling of human epidermis: unique signature of SCN9A painful neuropathy.Brain : a journal of neurology · 2023Article
- A novel co-target of ACY1 governing plasma membrane translocation of SphK1 contributes to inflammatory and neuropathic pain.iScience · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
At present, chronic post-surgical pain (CPSP) is difficult to prevent and cure clinically because of our lack of understanding of its mechanisms. Surgical injury induces the upregulation of voltage-gated sodium channel Nav1.7 in dorsal root ganglion (DRG) neurons, suggesting that Nav1.7 is involved in the development of CPSP. However, the mechanism leading to persistent dysregulation of Nav1.7 is largely unknown. Given that nerve growth factor (NGF) induces a long-term increase in the neuronal hyperexcitability after injury, we hypothesized that NGF might cause the long-term dysregulation of Nav1.7. In this study, we aimed to investigate whether Nav1.7 regulation by NGF is involved in CPSP and thus contributes to the specific mechanisms involved in the development of CPSP. Using conditional nociceptor-specific Nav1.7 knockout mice, we confirmed the involvement of Nav1.7 in NGF-induced pain and identified its role in the maintenance of pain behavior during long-term observations (up to 14 days). Using western blot analyses and immunostaining, we showed that NGF could trigger the upregulation of Nav1.7 expression and thus support the development of CPSP in rats. Using pharmacological approaches, we showed that the increase of Nav1.7 might be partly regulated by an NGF/TrkA-SGK1-Nedd4-2-mediated pathway. Furthermore, reversing the upregulation of Nav1.7 in DRG could alleviate spinal sensitization. Our results suggest that the maintained upregulation of Nav1.7 triggered by NGF contributes to the development of CPSP. Attenuating the dysregulation of Nav1.7 in peripheral nociceptors may be a strategy to prevent the transition from acute post-surgical pain to CPSP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.