{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T17:44:03Z","timestamp":1790963043011,"version":"4.1.0"},"reference-count":170,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T00:00:00Z","timestamp":1759276800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Interstitial lung disease (ILD) is a significant extra-articular complication of rheumatoid arthritis (RA), characterized by high prevalence and mortality rates. Although advancements have been made in understanding its potential mechanisms, the pathogenesis of RA-associated ILD remains incompletely understood. Recent research has shed light on roles of various disease-related signaling pathways, including TGF-\u03b2\/SMAD, JAK\/STAT, PI3K\u2013Akt, Wnt\/\u03b2-catenin, and NF-\u03baB, which are implicated in development of both RA and lung fibrosis. These shared pathways, which drive inflammatory cytokine production and fibroblast proliferation, offer promising opportunities for therapeutic intervention, including pathway-specific inhibition and drug repurposing. Furthermore, the growing identification of potential biomarkers for early detection and severity assessment in RA-ILD patients holds promise for improving clinical management and guiding treatment strategies. Current treatments fall short in effectively halting the progression of lung fibrosis. 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