Chemical Mediators' Expression Associated with the Modulation of Pain in Rheumatoid Arthritis.

Rheumatoid arthritis chemical mediators ionic channels nociception pain transcription factors

Journal

Current medicinal chemistry
ISSN: 1875-533X
Titre abrégé: Curr Med Chem
Pays: United Arab Emirates
ID NLM: 9440157

Informations de publication

Date de publication:
2020
Historique:
received: 28 02 2019
revised: 12 07 2019
accepted: 18 07 2019
pubmed: 20 8 2019
medline: 20 1 2021
entrez: 18 8 2019
Statut: ppublish

Résumé

The management of pain in patients with rheumatoid arthritis (RA) is a complex subject due to the autoimmune nature of the pathology. Studies have shown that chemical mediators play a fundamental role in the determination, susceptibility and modulation of pain at different levels of the central and peripheral nervous system, resulting in interesting novel molecular targets to mitigate pain in patients with RA. However, due to the complexity of pain physiology in RA cand the many chemical mediators, the results of several studies are controversial. The aim of this study was to identify the chemical mediators that are able to modulate pain in RA. In this review, a search was conducted on PubMed, ProQuest, EBSCO, and the Science Citation index for studies that evaluated the expression of chemical mediators on the modulation of pain in RA. Few studies have highlighted the importance of the expression of some chemical mediators that modulate pain in patients with rheumatoid arthritis. The expression of TRPV1, ASIC-3, and TDV8 encode ionic channels in RA and modulates pain, likewise, the transcription factors in RA, such as TNFα, TGF-β1, IL-6, IL-10, IFN-γ, IL-1b, mTOR, p21, caspase 3, EDNRB, CGRPCALCB, CGRP-CALCA, and TAC1 are also directly involved in pain perception. The expression of all chemical mediators is directly related to RA and the modulation of pain by a complex intra and extracellular signaling pathway, however, transcription factors are involved in modulating acute pain, while the ionic channels are involved in chronic pain in RA.

Sections du résumé

BACKGROUND
The management of pain in patients with rheumatoid arthritis (RA) is a complex subject due to the autoimmune nature of the pathology. Studies have shown that chemical mediators play a fundamental role in the determination, susceptibility and modulation of pain at different levels of the central and peripheral nervous system, resulting in interesting novel molecular targets to mitigate pain in patients with RA. However, due to the complexity of pain physiology in RA cand the many chemical mediators, the results of several studies are controversial.
OBJECTIVE
The aim of this study was to identify the chemical mediators that are able to modulate pain in RA.
METHOD
In this review, a search was conducted on PubMed, ProQuest, EBSCO, and the Science Citation index for studies that evaluated the expression of chemical mediators on the modulation of pain in RA.
RESULTS
Few studies have highlighted the importance of the expression of some chemical mediators that modulate pain in patients with rheumatoid arthritis. The expression of TRPV1, ASIC-3, and TDV8 encode ionic channels in RA and modulates pain, likewise, the transcription factors in RA, such as TNFα, TGF-β1, IL-6, IL-10, IFN-γ, IL-1b, mTOR, p21, caspase 3, EDNRB, CGRPCALCB, CGRP-CALCA, and TAC1 are also directly involved in pain perception.
CONCLUSION
The expression of all chemical mediators is directly related to RA and the modulation of pain by a complex intra and extracellular signaling pathway, however, transcription factors are involved in modulating acute pain, while the ionic channels are involved in chronic pain in RA.

Identifiants

pubmed: 31419924
pii: CMC-EPUB-100284
doi: 10.2174/0929867326666190816225348
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

6208-6218

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

José Luis Cortes-Altamirano (JL)

Neuropharmacology, Departament of Neurosciences, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389 Ciudad de México, México
Department of Chiropractic, State University of the Valley of Ecatepec (UNEVE), Ecatepec de Morelos, Estado de México, México

Abril Morraz-Varela (A)

Neuropharmacology, Departament of Neurosciences, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389 Ciudad de México, México

Samuel Reyes-Long (S)

Neuropharmacology, Departament of Neurosciences, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389 Ciudad de México, México
Escuela Superior de Medicina, Instituto Politécnico Nacional (IPN), Ciudad de México, México

Marwin Gutierrez (M)

División de Enfermedades Musculoesqueléticas y Reumáticas, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra” (INR) Secretaría de Salud (SSA), Ciudad de México, México

Cindy Bandala (C)

Neuropharmacology, Departament of Neurosciences, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389 Ciudad de México, México
Escuela Superior de Medicina, Instituto Politécnico Nacional (IPN), Ciudad de México, México

Denise Clavijo-Cornejo (D)

División de Enfermedades Musculoesqueléticas y Reumáticas, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra” (INR) Secretaría de Salud (SSA), Ciudad de México, México

Alfonso Alfaro-Rodriguez (A)

Neuropharmacology, Departament of Neurosciences, Instituto Nacional de Rehabilitación “Luis Guillermo Ibarra Ibarra”, Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389 Ciudad de México, México

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Classifications MeSH