Cellular Mechanisms of Rheumatoid Arthritis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 3646

Special Issue Editor


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Guest Editor
Rheumatology & Immune-Mediated Diseases (IRIDIS) group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain
Interests: rheumatic and musculoskeletal diseases (RMDs); rheumatoid arthritis; psoriatic arthritis; systemic lupus erythematosus; systemic sclerosis
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Dear Colleagues,

Rheumatoid arthritis (RA) is a complex autoimmune disease that mainly affects peripheral joints, causing the destruction of joint structure and, ultimately, joint deformity and disability. RA can also affect other organs, including skin, lung, heart, and vasculature, which contribute to the morbidity and mortality. Multiple cell types play a key role in RA, including immune cells (monocytes/macrophages, B cells, and T cells); fibroblast-like synoviocytes (FLS), which are the joint stromal cells; endothelial cells; and osteoclasts. Research performed during recent decades has improved knowledge of the cellular mechanisms involved in the pathogenesis of RA. However, there are some aspects that have not been fully elucidated, such as the interactions between different cell types, the effect of current therapies at molecular and cellular level, as well as the identification of novel targets that can modulate the functional role of these cell types.

This Special Issue will include basic and translational original articles and reviews focused on cellular mechanisms involved in the pathogenesis of RA and the effect of current and novel treatments on these mechanisms, which will allow a better understanding of the pathogenesis of RA.

Dr. Samuel García Pérez
Guest Editor

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Keywords

  • rheumatoid arthritis, immune cells
  • fibroblast-like synoviocytes
  • endothelial cells
  • osteoclasts
  • molecular mechanisms
  • cellular responses

Published Papers (1 paper)

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Review

28 pages, 1454 KiB  
Review
Pathogenesis of Extraarticular Manifestations in Rheumatoid Arthritis—A Comprehensive Review
by Joško Mitrović, Stela Hrkač, Josip Tečer, Majda Golob, Anja Ljilja Posavec, Helena Kolar Mitrović and Lovorka Grgurević
Biomedicines 2023, 11(5), 1262; https://doi.org/10.3390/biomedicines11051262 - 24 Apr 2023
Cited by 7 | Viewed by 3143
Abstract
Rheumatoid arthritis (RA) is among the most prevalent and debilitating autoimmune inflammatory chronic diseases. Although it is primarily characterized by destructive peripheral arthritis, it is a systemic disease, and RA-related extraarticular manifestations (EAMs) can affect almost every organ, exhibit a multitude of clinical [...] Read more.
Rheumatoid arthritis (RA) is among the most prevalent and debilitating autoimmune inflammatory chronic diseases. Although it is primarily characterized by destructive peripheral arthritis, it is a systemic disease, and RA-related extraarticular manifestations (EAMs) can affect almost every organ, exhibit a multitude of clinical presentations, and can even be asymptomatic. Importantly, EAMs largely contribute to the quality of life and mortality of RA patients, particularly substantially increased risk of cardiovascular disease (CVD) which is the leading cause of death in RA patients. In spite of known risk factors related to EAM development, a more in-depth understanding of its pathophysiology is lacking. Improved knowledge of EAMs and their comparison to the pathogenesis of arthritis in RA could lead to a better understanding of RA inflammation overall and its initial phases. Taking into account that RA is a disorder that has many faces and that each person experiences it and responds to treatments differently, gaining a better understanding of the connections between the joint and extra-joint manifestations could help to create new treatments and improve the overall approach to the patient. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Rheumatoid Arthritis)
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