{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,26]],"date-time":"2026-07-26T03:52:55Z","timestamp":1785037975935,"version":"3.55.0"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004775","name":"Natural Science Foundation of Gansu Province","doi-asserted-by":"publisher","award":["24JRRA923"],"award-info":[{"award-number":["24JRRA923"]}],"id":[{"id":"10.13039\/501100004775","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004775","name":"Natural Science Foundation of Gansu Province","doi-asserted-by":"publisher","award":["25YFFA055"],"award-info":[{"award-number":["25YFFA055"]}],"id":[{"id":"10.13039\/501100004775","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82260325"],"award-info":[{"award-number":["82260325"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Interstitial lung disease (ILD) is the most common and prognostically severe complication of idiopathic inflammatory myopathy (IIM), for which targeted treatments remain limited. Based on previous findings that neutrophil extracellular traps (NETs) are key mediators in IIM\u2010ILD pathogenesis and given the established role of interleukin\u201033 (IL\u201033) in promoting NETosis, we hypothesized.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated analyses of human IIM\u2010ILD samples with a myositis\u2010associated ILD (MAILD) mouse model employing IL\u201033 knockout (KO) and reconstitution strategies. The ERK pathway was inhibited in vivo with U0126. In vitro, IL\u201033 knockdown alveolar epithelial cells were challenged with NETs. Assessments included enzyme\u2010linked immunosorbent assay, immunohistochemistry and\/or immunofluorescence, Western blot, and RNA sequencing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Serum IL\u201033 levels were significantly elevated in patients with IIM\u2010ILD compared with healthy controls, with concurrent upregulation of IL\u201033 in lung tissues. MAILD mice similarly showed increased IL\u201033 expression, whereas IL\u201033 KO mice exhibited attenuated lung inflammation, improved alveolar architecture, and decreased collagen deposition. Administration of exogenous IL\u201033 restored ILD severity in IL\u201033 KO mice to wild\u2010type levels. The levels of p\u2010ERK and epithelial\u2010mesenchymal transition (EMT) markers (E\u2010Ca and \u03b1\u2010smooth muscle actin) correlated with IL\u201033 expression. U0126 reduced p\u2010ERK levels, suppressed EMT, and ameliorated both pulmonary inflammation and fibrosis. In vitro, NETs induced EMT and ERK activation in A549 cells, effects that were abolished upon IL\u201033 silencing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>IL\u201033 promotes IIM\u2010ILD progression by activating ERK\u2010mediate EMT, identifying the IL\u201033\/ERK signaling axis as a potential therapeutic target. These results provide mechanistic insight into IIM\u2010ILD pathogenesis and support translational strategies for precision intervention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.43453","type":"journal-article","created":{"date-parts":[[2025,11,25]],"date-time":"2025-11-25T11:17:04Z","timestamp":1764069424000},"page":"948-960","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Interleukin\u201033 Promotes Interstitial Lung Disease in Idiopathic Inflammatory Myopathy Via\n                    <scp>ERK<\/scp>\n                    \u2010Mediated Epithelial\u2010Mesenchymal Transition:\n                    <scp>ERK<\/scp>\n                    as a Potential Therapeutic Target"],"prefix":"10.1002","volume":"78","author":[{"given":"Jumei","family":"Yang","sequence":"first","affiliation":[{"name":"Cuiying Biomedical Research Center Lanzhou University Second Hospital  Lanzhou 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