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Biomolecules
Special Issues
Research Progress of Molecular Mechanisms in Rheumatoid Arthritis
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Research Progress of Molecular Mechanisms in Rheumatoid Arthritis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 4253

Special Issue Editor

Prof. Dr. Charles J. Malemud

E-Mail Website
Guest Editor
Department of Medicine, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH 44106-5076, USA
Interests: inflammation; apoptosis; arthritis; chondrocytes; matrix metalloproteinases; signal transduction; pro-inflammatory; anti-inflammatory & anabolic cytokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Rheumatoid arthritis (RA) is a chronic, progressive inflammatory disorder that manifests as a symmetric polyarthritis of small and large joints that may lead to joint and periarticular structural damage and the consequences of systemic inflammation and associated extra-articular manifestations and comorbidities. The pathogenesis of rheumatoid arthritis (RA) consists of the formation of synovial villi, inflammation, immune abnormalities, and bone–cartilage destruction. Despite the great advances in the knowledge of the pathogenesis of rheumatoid arthritis, many aspects remain to be clarified.

The Special Issue "Research Progress of Molecular Mechanisms in Rheumatoid Arthritis” will focus on the wide spectrum of molecular mechanisms involved in the pathogenesis and clinical expression of rheumatoid arthritis as well as their possible contribution to treatment response and precision medicine.

We invite authors to contribute to this Special Issue with original research and review articles focusing on, but not limited to, epigenetic mechanisms, cell death mechanisms, post-translational modifications, innate and adaptive immunity, and non-immune cells (synovial fibroblasts, osteoclasts, endothelial cells) and mechanisms of inflammation resolution.

We hope this Special Issue becomes a good collection for the understanding of the molecular and cellular mechanisms of RA development.

Prof. Dr. Charles J. Malemud
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • rheumatoid arthritis
  • post-translational modifications
  • inflammation
  • extra-articular manifestations
  • immune response
  • precision medicine

Published Papers (2 papers)

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16 pages, 3184 KiB  
Article
Altered CD39 and CD73 Expression in Rheumatoid Arthritis: Implications for Disease Activity and Treatment Response
by María Angels Ortiz, Cesar Diaz-Torné, Juan Jose De Agustin, Paula Estrada, Delia Reina, María Victoria Hernandez, Hye Sang, Carlos Zamora, Elisabet Cantó, Hector Corominas and Silvia Vidal
Biomolecules 2024, 14(1), 1; https://doi.org/10.3390/biom14010001 - 19 Dec 2023
Cited by 1 | Viewed by 1164
Abstract
In rheumatoid arthritis (RA) synovium, ATP, and ADP are released, sparking inflammation. Ectoenzymes CD39 and CD73 metabolize these purine nucleotides, generating anti-inflammatory adenosine. Therefore, dysregulated CD39 and CD73 expression may impact RA development. We assessed CD39 and CD73 expression in peripheral blood from [...] Read more.
In rheumatoid arthritis (RA) synovium, ATP, and ADP are released, sparking inflammation. Ectoenzymes CD39 and CD73 metabolize these purine nucleotides, generating anti-inflammatory adenosine. Therefore, dysregulated CD39 and CD73 expression may impact RA development. We assessed CD39 and CD73 expression in peripheral blood from 15 healthy controls (Cs) and 35 RA patients at baseline and after 3 and 6 months of tocilizumab treatment using flow cytometry. Additionally, ectoenzyme expression was examined on cultured T cells to understand activation and IL-6 effects. At baseline, RA patients exhibited a lower CD8+CD39−CD73+ cell percentage, which inversely correlated with DAS28. Additionally, they had lower percentages of Treg CD39+CD73+ and CD39−CD73− cells. Good responders tended to have lower B CD39+CD73+ cell percentages at baseline and 3 months. Additionally, Treg, CD8+ T and B cells inversely correlated with DAS28. T-cell activation increased CD39 and decreased CD73 expression, regardless of IL-6. IL-6 reduced IFNγ-secreting CD4+ T-cell percentage in Cs, but increased the percentage of IFNγ-secreting CD4+ and CD8+ T cells in RA patients. These findings indicate differing CD39 and CD73 expression in RA and Cs, influenced by T-cell activation and IL-6. Correlations between these molecules and RA activity suggest their role in dysregulated inflammation in RA. Full article
(This article belongs to the Special Issue Research Progress of Molecular Mechanisms in Rheumatoid Arthritis)
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16 pages, 4657 KiB  
Article
Low-Intensity Physical Exercise Decreases Inflammation and Joint Damage in the Preclinical Phase of a Rheumatoid Arthritis Murine Model
by Susana Aideé González-Chávez, Salma Marcela López-Loeza, Samara Acosta-Jiménez, Rubén Cuevas-Martínez, César Pacheco-Silva, Eduardo Chaparro-Barrera and César Pacheco-Tena
Biomolecules 2023, 13(3), 488; https://doi.org/10.3390/biom13030488 - 07 Mar 2023
Cited by 6 | Viewed by 2717
Abstract
Lifestyle modifications in preclinical Rheumatoid Arthritis (RA) could delay the ongoing pathogenic immune processes and potentially prevent its onset. Physical exercise (PE) benefits RA patients; however, its impact in reducing the risk of developing RA has scarcely been studied. The objective was to [...] Read more.
Lifestyle modifications in preclinical Rheumatoid Arthritis (RA) could delay the ongoing pathogenic immune processes and potentially prevent its onset. Physical exercise (PE) benefits RA patients; however, its impact in reducing the risk of developing RA has scarcely been studied. The objective was to describe the effects of low-intensity PE applied at the disease’s preclinical phase on the joints of DBA/1 mice with collagen-induced arthritis (CIA). Twelve mice with CIA were randomly distributed into two groups: the CIA-Ex group, which undertook treadmill PE, and the CIA-NoEx, which was not exercised. The effects of PE were evaluated through clinical, histological, transcriptomics, and immunodetection analyses in the mice’s hind paws. The CIA-Ex group showed lower joint inflammation and damage and a decreased expression of RA-related genes (Tnf Il2, Il10, Il12a, IL23a, and Tgfb1) and signaling pathways (Cytokines, Chemokines, JAK-STAT, MAPK, NF-kappa B, TNF, and TGF-beta). TNF-α expression was decreased by PE in the inflamed joints. Low-intensity PE in pre-arthritic CIA reduced the severity through joint down-expression of proinflammatory genes and proteins. Knowledge on the underlying mechanisms of PE in preclinical arthritis and its impact on reducing the risk of developing RA is still needed. Full article
(This article belongs to the Special Issue Research Progress of Molecular Mechanisms in Rheumatoid Arthritis)
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