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Molecular Research in Rheumatoid Arthritis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 March 2025 | Viewed by 736

Special Issue Editor


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Guest Editor
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1649-004 Lisboa, Portugal
Interests: inflammation; macrophage; neutrophil; leukocyte recruitment

Special Issue Information

Dear Colleagues,

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease. It is estimated to affect around 1% of the world’s population. RA patients can still face a decreased quality of life and lifespan. The etiology of this disease is, so far, incompletely understood and clarified. It is currently accepted that RA initiation and progression involves the interplay of risk factors that render the host susceptible to the disease, a breach of immune tolerance, autoantibody production, a self-perpetuating inflammatory response, and dysregulated innate and adaptive immune responses. Primarily, RA affects the synovial tissue of small joints, where the hyperproliferation of synovial cells and infiltration of immune cells lead to synovitis and can subsequently contribute to cartilage and bone destruction. This leads to the progressive damage of the musculoskeletal system and contributes to decreased physical function. As well as this, RA can also impact the function of almost all other organs in the body, evident from the myriad of systemic manifestations associated with this disease. Recent decades have witnessed an impressive advancement in our knowledge of the cellular and molecular mechanisms enrolled in RA pathophysiology. Yet, a lot remains to be clarified and understood. This Special Issue intends to provide the reader with a glimpse of the latest advances in the cellular and molecular mechanisms underlying RA pathogenesis, and on how these may hopefully translate towards better therapeutical approaches for RA treatment. Within this scope, authors are invited to contribute with original research or review papers.

Dr. Ângelo Calado
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • rheumatoid arthritis
  • synovium
  • autoimmunity
  • rheumatology
  • omics

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Published Papers (1 paper)

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Research

14 pages, 868 KiB  
Article
Intestinal Dysbiosis, Tight Junction Proteins, and Inflammation in Rheumatoid Arthritis Patients: A Cross-Sectional Study
by Arkaitz Mucientes, José Manuel Lisbona-Montañez, Natalia Mena-Vázquez, Patricia Ruiz-Limón, Sara Manrique-Arija, Aimara García-Studer, Fernando Ortiz-Márquez and Antonio Fernández-Nebro
Int. J. Mol. Sci. 2024, 25(16), 8649; https://doi.org/10.3390/ijms25168649 - 8 Aug 2024
Viewed by 543
Abstract
Recent studies point to intestinal permeability as an important factor in the establishment and development of rheumatoid arthritis (RA). Tight junctions (TJs) play a major role in intestinal homeostasis. The alteration of this homeostasis is related to RA. Furthermore, RA patients present dysbiosis [...] Read more.
Recent studies point to intestinal permeability as an important factor in the establishment and development of rheumatoid arthritis (RA). Tight junctions (TJs) play a major role in intestinal homeostasis. The alteration of this homeostasis is related to RA. Furthermore, RA patients present dysbiosis and a lower microbiota diversity compared to healthy individuals. A cross-sectional study including RA patients and sex- and age-matched healthy controls was performed. The quantification of TJ proteins was carried out by ELISA. Gut microbiota was evaluated by NGS platform Ion Torrent S. The inflammatory variables included were DAS28, CRP, inflammatory cytokines (IL-6, IL-1, TNF-α) and oxidised LDL. Claudin-1 levels showed significant differences between groups. Results evidenced a correlation between claudin-1 values and age (r: −0.293; p < 0.05), IL6 (r: −0.290; p < 0.05) and CRP (r: −0.327; p < 0.05), and between zonulin values and both age (r: 0.267; p < 0.05) and TNFα (r: 0.266; p < 0.05). Moreover, claudin-1 and CRP levels are related in RA patients (β: −0.619; p: 0.045), and in patients with high inflammatory activity, the abundance of the genus Veillonella is positively associated with claudin-1 levels (β: 39.000; p: 0.004). Full article
(This article belongs to the Special Issue Molecular Research in Rheumatoid Arthritis)
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Figure 1

Figure 1
<p>Schematic representation of the gastrointestinal barrier, highlighting the tight junction (TJ) proteins analysed. Zonulin (red) modulates intestinal permeability by regulating TJ disassembly. Occludin (green) and claudin-1 (yellow) are structural proteins of the TJ that co-ordinately maintain the integrity and selective permeability of the barrier. When zonulin binds the EGFR (dark blue) and PAR2 (dark green) receptors, it activates a cascade of reactions that ultimately result in the displacement of occludin and claudin-1, leading to loosening of the TJs (2). When zonulin signalling stops, the TJs return to their closed basal state (1).</p>
Full article ">Figure 2
<p>Concentration of the distinct tight junction proteins analysed in faeces. Red: rheumatoid arthritis (RA) patients; blue: healthy controls. Data are shown as mean ± standard deviation for claudin-1 and median (p25–p75) for occludin and zonulin. Significance level: * <span class="html-italic">p</span> ≤ 0.05.</p>
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