ArticleFrontiers in molecular neuroscience2022
Protein Tyrosine Phosphatase Receptor Type D Regulates Neuropathic Pain After Nerve Injury
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Research Progress on Regulating Neuroinflammation After Spinal Cord Injury by Targeting the cGAS-STING Pathway.Neuromolecular medicine · 2026Review
- Persistent interferon signaling causes sensory neuron plasticity and pain before and during arthritis.Nature neuroscience · 2026Article
- Spreading depolarization activates the cGAS-STING pathway and drives cranial nociception: therapeutic potential of STING modulation.The journal of headache and pain · 2026Article
- Innate immune pathway activated mesenchymal stromal cells improve function and histologic outcomes in a rodent osteoarthritis model.Frontiers in bioengineering and biotechnology · 2025Article
- Innate immune pathway activation to modulate mesenchymal stromal cell (MSC) interactions with synovium and cartilage.Frontiers in bioengineering and biotechnology · 2025Article
- STING-Pathway Inhibiting Nanoparticles (SPINs) as a Platform for Treatment of Inflammatory Diseases.ACS applied bio materials · 2024Review
- STINGing away the pain: the role of interferon-stimulated genes.The Journal of clinical investigation · 2024Article
- Induction of antiviral interferon-stimulated genes by neuronal STING promotes the resolution of pain in mice.The Journal of clinical investigation · 2024Article
- Vinorelbine causes a neuropathic pain-like state in mice via STING and MNK1 signaling associated with type I interferon induction.iScience · 2024Article
- Exploring blood transcriptomic signatures in patients with herpes zoster and postherpetic neuralgia.Frontiers in cellular and infection microbiology · 2024Article
- The Role of cGAS-STING Signalling in Metabolic Diseases: from Signalling Networks to Targeted Intervention.International journal of biological sciences · 2024Review
- STING-IFN-I pathway relieves incision induced acute postoperative pain via inhibiting the neuroinflammation in dorsal root ganglion of rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- STING controls opioid-induced itch and chronic itch via spinal tank-binding kinase 1-dependent type I interferon response in mice.Journal of neuroinflammation · 2023Article
- Blockade of Cholecystokinin Type 2 Receptors Prevents the Onset of Vincristine-Induced Neuropathy in Mice.Pharmaceutics · 2022Article
- Mechanism and effects of STING-IFN-I pathway on nociception: A narrative review.Frontiers in molecular neuroscience · 2022Review
- What role of the cGAS-STING pathway plays in chronic pain?Frontiers in molecular neuroscience · 2022Review
- Mitochondrial DAMPs produce inflammatory hyperalgesia via stimulator of interferon genes (STING) activation in DRG neurons.Molecular painArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is usually caused by injury or dysfunction of the somatosensory system, and medicine is a common way of treatment. Currently, there are still no satisfactory drugs, like opioids and lidocaine, which carry a high risk of addiction. Protein tyrosine phosphatase receptor type D (PTPRD) is a known therapeutic target in addiction pathways and small molecule inhibitors targeting it, such as 7-butoxy illudalic acid analog (7-BIA), have recently been developed to tackle addition. PTPRD is also upregulated in the dorsal root ganglion (DRG) in a rat model of neuropathic pain, but is not yet clear whether PTPRD contributes to the development of neuropathic pain. Here, we established a chronic constriction injury (CCI) and evaluated PTPRD expression and its association with neuropathic pain. PTPRD expression was found to gradually increase after CCI in DRGs, and its expression was concomitant with the progressive development of hypersensitivity as assessed by both mechanical and thermal stimuli. Both PTPRD knockdown and administration of PTPRD inhibitor 7-BIA alleviated CCI-induced neuropathic pain while upregulating STING and IFN-α in the DRG. Treatment with H-151, a STING inhibitor, abolished the analgesic effects of PTPRD knockdown. Taken together, our study suggests that increased levels of PTPRD in the DRG following CCI are involved in the development of neuropathic pain
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