Academic Journal

Joint-brain communication in rheumatoid arthritis: glial mechanisms, pain phenotypes, and translational evidence.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Joint-brain communication in rheumatoid arthritis: glial mechanisms, pain phenotypes, and translational evidence.
Συγγραφείς: Guo D; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Xu K; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Xiao L; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Li H; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Li Z; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Pan Y; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China., Zhang H; Department of Joint Surgery, Honghui Hospital, Xi'an Jiaotong University, Xi'an, China.
Πηγή: Frontiers in immunology [Front Immunol] 2026 Sep 29; Vol. 17, pp. 1889608. Date of Electronic Publication: 2026 Sep 29 (Print Publication: 2026).
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
Imprint Name(s): Original Publication: [Lausanne : Frontiers Research Foundation]
Ιατρικοί όροι (MeSH): Arthritis, Rheumatoid*/physiopathology , Arthritis, Rheumatoid*/immunology , Arthritis, Rheumatoid*/metabolism , Neuroglia*/metabolism , Neuroglia*/immunology , Brain*/physiopathology , Brain*/immunology , Brain*/metabolism , Joints*/immunology , Joints*/physiopathology , Pain*, Humans ; Animals ; Phenotype ; Translational Research, Biomedical
Περίληψη: Rheumatoid arthritis (RA) is a systemic autoimmune disease in which persistent pain, fatigue, cognitive impairment, depression, and anxiety may involve altered central nervous system (CNS) processing. This narrative review synthesizes preclinical and clinical evidence concerning proposed glial cell-mediated joint-brain communication in RA. Joint-derived neural inputs and systemic inflammatory signals may communicate with the CNS through humoral, cellular, neural, neuroendocrine, and neurovascular pathways. Preclinical studies implicate microglia and astrocytes in neuroinflammatory responses, spinal central sensitization, impaired hippocampal plasticity, and neurovascular alterations. Human studies associate systemic inflammation with altered brain connectivity and CNS-related symptoms. Disease-modifying antirheumatic treatment, particularly tumor necrosis factor inhibition, has been associated with improvements in selected CNS-related outcomes. Adjunctive symptom management includes phenotype-guided analgesic approaches, rehabilitation, and psychological and sleep-focused interventions. Translational research explores glial modulators, pathway-specific interventions, vagal neuromodulation, neuroimaging, cerebrospinal fluid markers, and multidimensional patient stratification. The proposed joint-brain framework highlights the value of assessing inflammation alongside pain phenotype, cognition, mood, fatigue, sleep, and function. Future human studies should evaluate whether mechanistic and biomarker findings can improve individualized treatment selection and clinical outcomes.
(Copyright © 2026 Guo, Xu, Xiao, Li, Li, Pan and Zhang.)
Competing Interests: The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Contributed Indexing: Keywords: central sensitization; glial cells; joint–brain axis; neuroinflammation; rheumatoid arthritis
Entry Date(s): Date Created: 20261014 Date Completed: 20261014 Latest Revision: 20261015
Update Code: 20261015
PubMed Central ID: PMC13659651
DOI: 10.3389/fimmu.2026.1889608
PMID: 42872037
Βάση Δεδομένων: MEDLINE