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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Nociceptive related microRNAs and their role in rheumatoid arthritis
S Reyes-Long1,2, J L Cortes-Altamirano1, D Clavijio-Cornejo3
1Department of Neurosciences, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Calzada México-Xochimilco 289, Col. Arenal de Guadalupe, Del. Tlalpan, 14389, Mexico City, Mexico.
Abstract:
Rheumatoid Arthritis (RA) is an autoimmune disease with unknown etiology and a global incidence around 1%, a positive family history increases the risk of RA roughly three to five times. Pain is one of the first symptoms to appear in this disease. MicroRNAs (miRNAs) belong to the class of small non-coding RNAs; they regulate multiple cellular processes including embryonic development, cellular proliferation, differentiation and apoptosis among others. A great deal of evidence points to the employment of miRNAs as therapeutic targets and biomarkers for several pathologies. The main objective of this Review is to assess how miRNAs participate in the pathogenesis of RA. Two advanced searches were conducted in databases, one using "micro-RNA" and "rheumatoid arthritis" as key words, and another one with "micro-RNA", "pain" and "nociception". In this Review, we describe how six miRNAs: miR-16-5p, miR-23b-3b, miR-124-3p, miR-146a-5p, miR-155-5p and miR-223-3p, involved in the modulation and transmission of the nociceptive input are unregulated in RA patients. Key molecular pathways involved in nociception, inflammation and autoimmune responses, are regulated by these miRNAs; the NF-κB, TNF-α, interleukins and TLR4. By means of gene repression, the miRNAs here described modulate the nociceptive process as well as the autoimmune response that characterize this disease.
Insights
MicroRNAs (miRNAs) are implicated in rheumatoid arthritis (RA) pathogenesis. Six specific miRNAs are dysregulated in RA patients, influencing pain and autoimmune responses through gene repression.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Rheumatoid Arthritis (RA) is a prevalent autoimmune disease affecting approximately 1% of the global population.
- Pain is a primary early symptom of RA, significantly impacting patient quality of life.
- MicroRNAs (miRNAs) are small non-coding RNAs crucial for regulating cellular functions and are implicated in various diseases.
Purpose of the Study:
- To investigate the role of miRNAs in the pathogenesis of Rheumatoid Arthritis (RA).
- To identify specific miRNAs involved in pain modulation and autoimmune responses in RA patients.
Main Methods:
- Conducted comprehensive literature searches in scientific databases using keywords related to "micro-RNA", "rheumatoid arthritis", "pain", and "nociception".
- Reviewed studies focusing on the expression and function of miRNAs in the context of RA and pain pathways.
Main Results:
- Identified six specific miRNAs (miR-16-5p, miR-23b-3b, miR-124-3p, miR-146a-5p, miR-155-5p, miR-223-3p) that are dysregulated in RA patients.
- These miRNAs modulate key molecular pathways including NF-κB, TNF-α, interleukins, and TLR4, which are central to nociception, inflammation, and autoimmune responses.
- Demonstrated that these miRNAs regulate nociceptive processes and autoimmune responses in RA through gene repression.
Conclusions:
- Specific miRNAs play a significant role in the pathogenesis of RA by influencing both pain signaling and autoimmune mechanisms.
- Dysregulation of miRNAs like miR-16-5p, miR-23b-3b, miR-124-3p, miR-146a-5p, miR-155-5p, and miR-223-3p contributes to RA symptoms and progression.
- These miRNAs represent potential therapeutic targets and biomarkers for Rheumatoid Arthritis.
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