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Through recruitment and activation of neutrophils from circulation, these macrophages promote the release of neutrophil extracellular traps (NETs) and generation of reactive oxygen species (ROS), leading to synovitis exacerbation and tissue damage. To disrupt this closely linked cycle, we present a mitochondria\u2010modulating nanosystem (NM@APDAase) targeting the inflammatory cascade for RA immunotherapy. The neutrophil membrane\u2010camouflaged nanomaterials are directed to inflamed joints, where the released AP39 effectively restores mitochondrial function by serving as a mild electron donor and uncoupler. This reprograms macrophages from a pro\u2010inflammatory to an anti\u2010inflammatory phenotype, thereby eliminating the primary source of inflammation. Notably, the co\u2010loaded DNase I and polydopamine scaffold work synergistically to clear pre\u2010existing NETs and scavenge ROS. In vivo studies demonstrate that NM@APDAase significantly alleviates RA pathology as evidenced by reduced inflammatory responses, mitigated cartilage erosion and reduced bone destruction. Our work highlights the promise of mitochondria\u2010modulating nanomaterials for treating RA through directed disruption of the inflammatory cascade.<\/jats:p>","DOI":"10.1002\/adhm.71846","type":"journal-article","created":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T07:28:16Z","timestamp":1792654096000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["A Mitochondria\u2010Modulating Nanosystem for Rheumatoid Arthritis Immunotherapy via Inflammatory Cascade Disruption"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-2439-5086","authenticated-orcid":false,"given":"Qingshui","family":"Wen","sequence":"first","affiliation":[{"name":"Department of Rheumatology Research Center of Clinical Medicine Research Center of Immunology Affiliated Hospital of Nantong University  Nantong China"},{"name":"Graduate School of Dalian Medical University  Dalian 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