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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 October 2025 | Viewed by 2909

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

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Keywords

  • rheumatoid arthritis
  • synovium
  • autoimmunity
  • rheumatology
  • omics

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Published Papers (2 papers)

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15 pages, 4162 KiB  
Article
The Identification of Novel Therapeutic Biomarkers in Rheumatoid Arthritis: A Combined Bioinformatics and Integrated Multi-Omics Approach
by Muhammad Hamza Tariq, Dia Advani, Buttia Mohamed Almansoori, Maithah Ebraheim AlSamahi, Maitha Faisal Aldhaheri, Shahad Edyen Alkaabi, Mira Mousa and Nupur Kohli
Int. J. Mol. Sci. 2025, 26(6), 2757; https://doi.org/10.3390/ijms26062757 - 19 Mar 2025
Viewed by 580
Abstract
Rheumatoid arthritis (RA) is a multifaceted autoimmune disease that is marked by a complex molecular profile influenced by an array of factors, including genetic, epigenetic, and environmental elements. Despite significant advancements in research, the precise etiology of RA remains elusive, presenting challenges in [...] Read more.
Rheumatoid arthritis (RA) is a multifaceted autoimmune disease that is marked by a complex molecular profile influenced by an array of factors, including genetic, epigenetic, and environmental elements. Despite significant advancements in research, the precise etiology of RA remains elusive, presenting challenges in developing innovative therapeutic markers. This study takes an integrated multi-omics approach to uncover novel therapeutic markers for RA. By analyzing both transcriptomics and epigenomics datasets, we identified common gene candidates that span these two omics levels in patients diagnosed with RA. Remarkably, we discovered eighteen multi-evidence genes (MEGs) that are prevalent across transcriptomics and epigenomics, twelve of which have not been previously linked directly to RA. The bioinformatics analyses of the twelve novel MEGs revealed they are part of tightly interconnected protein–protein interaction networks directly related to RA-associated KEGG pathways and gene ontology terms. Furthermore, these novel MEGs exhibited direct interactions with miRNAs linked to RA, underscoring their critical role in the disease’s pathogenicity. Overall, this comprehensive bioinformatics approach opens avenues for identifying new candidate markers for RA, empowering researchers to validate these markers efficiently through experimental studies. By advancing our understanding of RA, we can pave the way for more effective therapies and improved patient outcomes. Full article
(This article belongs to the Special Issue Molecular Research in Rheumatoid Arthritis)
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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 1908
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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