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Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Review Article

Immunometabolism Dysfunction in the Pathophysiology and Treatment of Rheumatoid Arthritis

Author(s): Maryam Masoumi, Nader Hashemi, Fatemeh Moadab, Mojtaba Didehdar, Rahim Farahani, Hossein Khorramdelazad, Amirhossein Sahebkar*, Thomas P. Johnston and Jafar Karami*

Volume 30, Issue 27, 2023

Published on: 10 November, 2022

Page: [3119 - 3136] Pages: 18

DOI: 10.2174/0929867329666220907151213

Price: $65

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial hyperplasia and joint damage. Systemic complications and progressive disability are burdens that lead to a significant socio-economic costs in patients with RA. Current RA biomarkers used in predicting, diagnosing, and monitoring the treatment of the disease have not been very successful. Moreover, only 60% of patients show a satisfactory response to current biological and conventional therapies. Studies on immunometabolism have suggested that dysregulated enzymes, transcription factors, metabolites, and metabolic pathways could be considered potential therapeutic targets for the treatment of RA. Factors such as the high concentration of various intermediate molecules arising from metabolism, hypoxia, lack of nutrients, and other metabolic alterations affect local immune responses and preserve a state of chronic inflammation in synovial tissues. Fortunately, in vitro and in vivo studies have shown that targeting specific metabolic pathways is associated with a decreased level of inflammation. Specifically, targeting metabolic intermediates, such as succinate or lactate, has shown promising clinical outcomes in RA treatment. These findings open an avenue for the identification of novel biomarkers for diagnosis, prognosis, and determining the success of various treatments in RA patients, as well as the discovery of new therapeutic targets.

Keywords: Rheumatoid, arthritis, immunometabolism, autoimmune disease, synovial hyperplasia, RA biomarkers.

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