ArticleBioMed research international2020
The Actions and Mechanisms of P2X7R and p38 MAPK Activation in Mediating Bortezomib-Induced Neuropathic Pain.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- P2X7 receptors promote atrial remodeling and atrial fibrillation susceptibility via reactive oxygen species-mediated mitogen-activated protein kinase signaling activation.Journal of cell communication and signaling · 2026Article
- P2X7 Receptor as a Therapeutic Target for Neuropathic Pain: From Mechanisms to Translational Strategies.Current pain and headache reports · 2026Review
- Gastrodin alleviates bortezomib-induced peripheral neuropathy by inhibiting NF-κB/NLRP3 pathway-mediated microglial inflammation.The Korean journal of pain · 2026Article
- Review
- Inhibition of P2X7 receptor in satellite glial cells contributes to electroacupuncture's analgesia in rats with CFA-induced inflammatory pain.Chinese medicine · 2025Article
- KNN-based frequency-adjustable ferroelectric heterojunction and biomedical applications.Nature communications · 2025Article
- Resident Macrophages in the Cervical Sympathetic Ganglia Participate in P2Y12 Receptor Mediated Diabetic Cardiac Autonomic Neuropathy.Molecular neurobiology · 2025Article
- The role of purinergic signaling in acupuncture-mediated relief of neuropathic and inflammatory pain.Purinergic signalling · 2025Review
- Enhanced exosome secretion regulated by microglial P2X7R in the medullary dorsal horn contributes to pulpitis-induced pain.Cell & bioscience · 2025Article
- Bortezomib-induced peripheral neuropathy: from molecular mechanisms to clinical management.Frontiers in pharmacology · 2025Review
- Expression in skin biopsies supports genetic evidence linking CAMKK2, P2X7R and P2X4R with HIV-associated sensory neuropathy.Journal of neurovirology · 2023Article
- From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review.International journal of molecular sciences · 2022Review
- Ligand-gated ion channel P2X7 regulates hypoxia-induced factor-1α mediated pain induced by dental pulpitis in the medullary dorsal horn.Frontiers in molecular neuroscience · 2022Article
- Paeoniflorin Ameliorates BiPN by Reducing IL6 Levels and Regulating PARKIN-Mediated Mitochondrial Autophagy.Drug design, development and therapy · 2022Article
- Vincristine- and bortezomib-induced neuropathies - from bedside to bench and back.Experimental neurology · 2021Review
- Pathological Mechanisms of Bortezomib-Induced Peripheral Neuropathy.International journal of molecular sciences · 2021Review
- Neuroinflammatory Process Involved in Different Preclinical Models of Chemotherapy-Induced Peripheral Neuropathy.Frontiers in immunology · 2020Review
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
The proteasome inhibitor bortezomib (BTZ) is a potent first-line anticancer drug for multiple myeloma; nonetheless, it induced peripheral neuropathy. It has been suggested that many cytokines may play a role in mediating neuropathic pain, but the underlying molecular mechanism is not fully understood. Recent studies have shown that neuropathic pain is closely related to the purinergic ligand-gated ion channel 7 receptor (P2X7R), one of the P2X receptors, which is richly expressed in glial cells. P2X7-p38 pathway is correlated with microglia- and satellite glial cell- (SGC-) mediated neuropathic pain. However, the association of P2X7R and p38MAPK in mediating BTZ-induced neuropathic pain remains unclear. In this study, the relationship between P2X7R activation and p38 phosphorylation in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) in the development and maintenance of BTZ-induced neuropathic pain was elucidated. The results showed that BTZ increased mechanical thresholds in rats, accompanied with upregulation of P2X7R expression and p38MAPK phosphorylation, indicating that P2X7R and p38MAPK are key molecules in the development and maintenance of BTZ-induced neuropathic pain. Inhibiting p38MAPK phosphorylation with SB203580 resulted in downregulation of P2X7R expression levels. Inhibition of P2X7R with Brilliant Blue G (BBG) reversed neuropathic pain might decrease through the expression of tumor necrosis factor-
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