ReviewCellular & molecular biology letters2024
Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.
Review in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Epigenetic changes associated with the progression of prion disease in Syrian hamsters (Prion · 2026Article
- Neuroprotective activity of the α7-nAChR positive allosteric modulator PNU-120596 on short term outcomes after traumatic brain injury.Experimental neurology · 2026Article
- Dietary allergen promotes sex-specific leukocyte trafficking and alters the brain immune cell populations in subclinically sensitized mice.Brain, behavior, and immunity · 2026Article
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- Article
- Cerebrospinal fluid proteomic signatures revealResearch square · 2026Article
- Electroacupuncture alleviates migraine through CXCL13/CXCR5-mediated communication.Chinese medicine · 2026Article
- CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain.Journal of neuroinflammation · 2026Article
- Electroacupuncture ameliorates incisional pain via suppressing IL-33 signaling-related macrophage infiltration and ROS overproduction in incised skin.Chinese medicine · 2026Article
- Immune remodeling and metabolic reprogramming in chronic fatigue: insights into GPCR signaling and epigenetic regulation.Frontiers in immunology · 2026Review
- CXCL13 and IL-33 as Immunomodulatory Adjuvants Combined with Respiratory Syncytial Virus Fusion (RSV F) Protein to Enhance Mucosal RSV Vaccination.Infection and drug resistance · 2026Review
- C-X-C motif chemokine ligand 13 and the C-X-C motif chemokine receptor 5-c-Jun N-terminal kinase-nuclear factor kappa B-matrix metalloproteinase 9 axis in oral squamous cell carcinoma metastasis.Journal of dental sciences · 2026Article
- The function of chemokine-driven glial-neuronal interaction in chronic pain.Frontiers in neuroscience · 2026Review
- Identification of T cell stress response state (TScientific reports · 2025Article
- Epigenetic Changes Associated with the Progression of Prion Disease in Syrian Hamsters (Mesocricetus auratus).Research square · 2025Article
- CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025Review
- Dural ectopic lymphatic structures accumulate during aging and exhibit dysregulation in neurodegenerative diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Follistatin, A Novel Therapeutic Target for Chronic Pain.Neuroscience bulletin · 2025Article
- Environmental enrichment for neuropathic pain via modulation of neuroinflammation.Frontiers in molecular neuroscience · 2025Review
- Decoding pain chronification: mechanisms of the acute-to-chronic transition.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Chronic pain dramatically affects life qualities of the sufferers. It has posed a heavy burden to both patients and the health care system. However, the current treatments for chronic pain are usually insufficient and cause many unwanted side effects. Chemokine C-X-C motif ligand 13 (CXCL13), formerly recognized as a B cell chemokine, binds with the cognate receptor CXCR5, a G-protein-coupled receptor (GPCR), to participate in immune cell recruitments and immune modulations. Recent studies further demonstrated that CXCL13-CXCR5 signaling is implicated in chronic pain via promoting neuroimmune interaction and neuroinflammation in the sensory system. In addition, some latest work also pointed out the involvement of CXCL13-CXCR5 in the pathogenesis of certain neurological diseases, including ischemic stroke and amyotrophic lateral sclerosis. Therefore, we aim to outline the recent findings in regard to the involvement of CXCL13-CXCR5 signaling in chronic pain as well as certain neurological diseases, with the focus on how this chemokine signaling contributes to the pathogenesis of these neurological diseases via regulating neuroimmune interaction and neuroinflammation. Strategies that can specifically target CXCL13-CXCR5 signaling in distinct locations may provide new therapeutic options for these neurological diseases.
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Registered trials
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