{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T19:50:31Z","timestamp":1791316231950,"version":"4.3.1"},"reference-count":67,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,12,17]],"date-time":"2022-12-17T00:00:00Z","timestamp":1671235200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2022,12,17]],"date-time":"2022-12-17T00:00:00Z","timestamp":1671235200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Non\u2010alcoholic fatty liver disease (NAFLD) is a major health problem in Western countries and has become the most common cause of chronic liver disease. Although NAFLD is closely associated with obesity, inflammation, and insulin resistance, its pathogenesis remains unclear. The disease begins with excessive accumulation of triglycerides in the liver, which in turn leads to liver cell damage, steatosis, inflammation, and so on. P38\u03b3 is one of the four isoforms of P38 mitogen\u2010activated protein kinases (P38 MAPKs) that contributes to inflammation in different diseases. In this research, we investigated the role of P38\u03b3 in NAFLD. In vivo, a NAFLD model was established by feeding C57BL\/6J mice with a methionine\u2010 and choline\u2010deficient (MCD) diet and adeno\u2010associated virus (AAV9\u2010shRNA\u2010P38\u03b3) was injected into C57BL\/6J mice by tail vein for knockdown P38\u03b3. The results indicated that the expression level of P38\u03b3 was upregulated in MCD\u2010fed mice. Furthermore, the downregulation of P38\u03b3 significantly attenuated liver injury and lipid accumulation in mice. In vitro, mouse hepatocytes AML\u201012 were treated with free fatty acid (FFA). We found that P38\u03b3 was obviously increased in FFA\u2010treated AML\u201012 cells, whereas knockdown of P38\u03b3 significantly suppressed lipid accumulation in FFA\u2010treated AML\u201012 cells. Furthermore, P38\u03b3 regulated the Janus Kinase\u2010Signal transducers and activators of transcription (JAK\u2013STAT) signaling pathway. Inhibition of P38\u03b3 can inhibit the JAK\u2013STAT signaling pathway, thereby inhibiting lipid accumulation in FFA\u2010treated AML\u201012 cells. In conclusion, our results suggest that targeting P38\u03b3 contributes to the suppression of lipid accumulation in fatty liver disease.<\/jats:p>","DOI":"10.1096\/fj.202200939rr","type":"journal-article","created":{"date-parts":[[2022,12,17]],"date-time":"2022-12-17T08:24:45Z","timestamp":1671265485000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["P38\u03b3 modulates the lipid metabolism in non\u2010alcoholic fatty liver disease by regulating the\n                    <scp>JAK\u2013STAT<\/scp>\n                    signaling pathway"],"prefix":"10.1096","volume":"37","author":[{"given":"Yan","family":"Yao","sequence":"first","affiliation":[{"name":"Inflammation and Immune Mediated Diseases Laboratory of Anhui Province Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University  Hefei China"},{"name":"Institute for Liver Diseases of Anhui Medical University  Hefei 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