International Journal of Molecular Sciences

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Dear Colleagues,

Rheumatoid arthritis is the most common inflammatory arthritis, affecting 1–2% of the population. The disease is characterized by autoantibody production, synovial inflammation leading to the destruction of cartilage and bone, and systemic inflammation responsible for extra-articular manifestations. Despite the great advances in the knowledge of the pathogenesis of rheumatoid arthritis, many aspects remain to be clarified. The Special Issue “Molecular Mechanisms of 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, host–pathogen interactions, 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 will consider papers addressing these mechanisms from a pathogenic point of view and/or exploring potential biomarkers of clinical expression/severity of the disease and therapeutic response suggesting stratified treatment options and predictive biomarkers.

Dr. Francesca Romana Spinelli
Dr. Arbi Pecani
Guest Editors

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Related Special Issue

Published Papers (1 paper)

Research

10 pages, 11660 KiB

Open AccessArticle

Sustained Hypoxia Suppresses Joint Destruction in a Rat Model of Rheumatoid Arthritis via Negative Feedback of Hypoxia Inducible Factor-1α

by Kenta Kaihara, Shuji Nakagawa, Yuji Arai, Hiroaki Inoue, Shinji Tsuchida, Yuta Fujii, Yoichiro Kamada, Tsunao Kishida, Osam Mazda and Kenji Takahashi

Int. J. Mol. Sci. 2021, 22(8), 3898; https://doi.org/10.3390/ijms22083898 - 09 Apr 2021

Cited by 8 | Viewed by 2118

Abstract

Hypoxia inducible factor (HIF)-1α has been implicated in the pathogenesis of rheumatoid arthritis (RA). HIF-1α, which is expressed in hypoxia, is reversely suppressed in sustained hypoxia. Here, we investigated the inhibitory effect of hypoxia on arthritis by controlling HIF-1α. Rheumatoid fibroblast-like synoviocyte MH7A cells were cultured in a hypoxic incubator for up to 72 h to evaluate the expression of HIF-1. Furthermore, collagen-induced arthritis (CIA) model rats were maintained under 12% hypoxia in a hypoxic chamber for 28 days to evaluate the effect on arthritis. In MH7A cells, HIF-1α protein level increased at 3 h, peaked at 6 h, and subsequently decreased in a time-dependent manner. The transcription of pro-inflammatory cytokines increased at 1 h; however, they decreased after 3 h (p < 0.05). Deferoxamine-mediated activation of HIF-1α abolished the inhibitory effect of sustained hypoxia on pro-inflammatory cytokines. In the rat CIA model, the onset of joint swelling was delayed and arthritis was suppressed in the hypoxia group compared with the normoxia group (p < 0.05). Histologically, joint destruction was suppressed primarily in the cartilage. Thus, sustained hypoxia may represent a new safe, and potent therapeutic approach for high-risk patients with RA by suppressing HIF-1α expression. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Rheumatoid Arthritis 2.0)

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