{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T09:58:31Z","timestamp":1790675911907,"version":"4.1.0"},"reference-count":163,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:00:00Z","timestamp":1790640000000},"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. Pharmacol."],"abstract":"<jats:p>Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent synovitis, pannus formation, cartilage degradation, and bone erosion. Although conventional synthetic, biologic, and targeted synthetic disease-modifying antirheumatic drugs have improved disease control, many patients fail to achieve sustained remission, lose responsiveness over time, or develop treatment-limiting safety concerns. Fibroblast-like synoviocytes (FLSs) are increasingly recognized as long-lived pathogenic stromal cells that sustain synovial inflammation, promote matrix degradation, support osteoclastogenesis, and shape immune and vascular crosstalk within the rheumatoid joint. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome provides a mechanistic link between synovial stress responses and inflammatory amplification. In RA-FLSs, defined inflammatory, hypoxic and oxidative-stress conditions can induce NLRP3-related signaling, whereas other proposed triggers, including lysosomal injury, extracellular ATP and ion flux, are supported more strongly by broader synovial or general inflammasome evidence. Through caspase-1 activation, interleukin (IL)-1\u03b2 and IL-18 maturation, and gasdermin D-mediated pyroptotic signaling, NLRP3 can reinforce stromal inflammation and tissue-destructive synovial remodeling. In this review, we summarize canonical, non-canonical, and alternative mechanisms of NLRP3 inflammasome activation, with emphasis on their relevance to RA-FLS biology and the inflamed synovial niche. We discuss how NLRP3 signaling intersects with fibroblast heterogeneity, macrophage\u2013FLS crosstalk, endothelial activation, chondrocyte injury, osteoclastogenesis, and context-dependent pyroptosis. We further evaluate pharmacological strategies targeting the NLRP3 axis, including direct NLRP3 inhibitors, upstream stress modulators, caspase-1 or gasdermin D blockade, IL-1\u03b2\/IL-18 pathway inhibition, natural products, repurposed molecules, nanomedicine-based delivery, and rational combination regimens. Key translational issues include FLS specificity, synovial drug exposure, target engagement, chronic safety, biomarker-guided patient selection, and mechanism-aligned endpoints. An RA-FLS-centered view of NLRP3 targeting may help refine anti-inflammatory pharmacology and support the development of synovium-directed therapeutic strategies for selected patients with difficult-to-treat RA.<\/jats:p>","DOI":"10.3389\/fphar.2026.1955904","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T09:13:12Z","timestamp":1790673192000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting the NLRP3 inflammasome in rheumatoid arthritis fibroblast-like synoviocytes: pathogenic mechanisms, therapeutic strategies, and translational perspectives"],"prefix":"10.3389","volume":"17","author":[{"given":"Lunmin","family":"Bao","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, People\u2019s Hospital of Anshun City","place":["Anshun, China"]},{"name":"School of Clinical Laboratory Science, Guizhou Medical University","place":["Guiyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haibing","family":"Dai","sequence":"additional","affiliation":[{"name":"School of Clinical Laboratory Science, Guizhou Medical University","place":["Guiyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daoming","family":"Wang","sequence":"additional","affiliation":[{"name":"School of Clinical Laboratory Science, Guizhou Medical University","place":["Guiyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongmei","family":"Jiang","sequence":"additional","affiliation":[{"name":"School of Clinical Laboratory Science, Guizhou Medical University","place":["Guiyang, China"]},{"name":"Department of Medical Technology, Zunyi Medical and Pharmaceutical College","place":["Zunyi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,29]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"669","DOI":"10.3899\/jrheum.200367","article-title":"The prevalence of rheumatoid arthritis: a systematic review of population-based studies","volume":"48","author":"Almutairi","year":"2021","journal-title":"J. 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