Etiology and Pathogenesis of Rheumatoid Arthritis-Interstitial Lung Disease

Interstitial lung disease (ILD) is one of the most serious extra-articular complications of rheumatoid arthritis (RA), which increases the mortality of RA. Because the pathogenesis of RA-ILD remains poorly understood, appropriate therapeutic strategies and biomarkers have not yet been identified. Th...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-10, Vol.24 (19), p.14509
Main Authors: Kim, Yerin, Yang, Hyung-In, Kim, Kyoung-Soo
Format: Article
Language:English
Subjects:
Age
Breastfeeding & lactation
Cohort analysis
Females
Genomes
Lung diseases
Lungs
Males
Medical prognosis
Mortality
Mutation
Pathogenesis
Patients
Pneumonia
Pulmonary fibrosis
Review
Rheumatoid arthritis
Risk factors
Tomography
Womens health
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Summary:Interstitial lung disease (ILD) is one of the most serious extra-articular complications of rheumatoid arthritis (RA), which increases the mortality of RA. Because the pathogenesis of RA-ILD remains poorly understood, appropriate therapeutic strategies and biomarkers have not yet been identified. Thus, the goal of this review was to summarize and analyze the reported data on the etiology and pathogenesis of RA-ILD. The incidence of RA-ILD increases with age, and is also generally higher in men than in women and in patients with specific genetic variations and ethnicity. Lifestyle factors associated with an increased risk of RA-ILD include smoking and exposure to pollutants. The presence of an anti-cyclic citrullinated peptide antibody, high RA disease activity, and rheumatoid factor positivity also increase the risk of RA-ILD. We also explored the roles of biological processes (e.g., fibroblast–myofibroblast transition, epithelial–mesenchymal transition, and immunological processes), signaling pathways (e.g., JAK/STAT and PI3K/Akt), and the histopathology of RA involved in RA-ILD pathogenesis based on published preclinical and clinical models of RA-ILD in animal and human studies.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241914509