{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T23:04:57Z","timestamp":1788995097798,"version":"build-2803163510"},"reference-count":79,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,4,18]],"date-time":"2023-04-18T00:00:00Z","timestamp":1681776000000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Skin Research and Technology"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>As a common skin disease, psoriasis is related to inflammation and immune response. Due to the frequent recurrence of psoriasis, the treatment of psoriasis remains a clinical challenge. As an effective tumor necrosis factor\u2010alpha (TNF\u2010\u03b1) inhibitor, etanercept has been used for the treatment of psoriasis. However, some patients with psoriasis have no response to etanercept or discontinue treatment. To improve the therapeutic effect of etanercept, searching the potential biomarkers and investigating the related mechanisms of etanercept in the treatment of psoriasis are vital.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>We stimulated HaCaT cells with lipopolysaccharide (LPS) to generate cellular psoriatic changes and established an imiquimod (IMQ)\u2010induced psoriasis\u2010like mouse model, and then used an etanercept to treat cell and mouse model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Etanercept alleviated IMQ\u2010induced pathological changes and inflammation, and it also decreased the protein expression of high mobility group box 1 (HMGB1), receptor for advanced glycation end\u2010products, and toll\u2010like receptor 4. Moreover, the results of in vitro experiments showed that etanercept inhibited proliferation and inflammation, and promoted cell cycle arrest and apoptosis in LPS\u2010treated HaCaT cells. Knockdown of HMGB1 further enhanced the inhibitory effects of etanercept on LPS\u2010treated HaCaT cell viability and inflammation, while overexpression of HMGB1 notably reversed the inhibitory effects of etanercept on LPS\u2010induced HaCaT cell viability and inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Etanercept inhibited proliferation and inflammation and promoted cell cycle arrest and apoptosis in LPS\u2010induced HaCaT cells, and etanercept ameliorated inflammation in a psoriasis\u2010like mouse model.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/srt.13329","type":"journal-article","created":{"date-parts":[[2023,4,19]],"date-time":"2023-04-19T01:17:28Z","timestamp":1681867048000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway"],"prefix":"10.1111","volume":"29","author":[{"given":"Shu","family":"Li","sequence":"first","affiliation":[{"name":"Department of Dermatology Taizhou People's Hospital  Taizhou P. 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