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In pancreatitis, ferroptosis promotes disease progression and organ damage by regulating oxidative stress and inflammatory response. Here, ferroptosis was significantly elevated in the AP rat model and participated in regulating disease progression. Meanwhile, the expression of S100A11 was significantly upregulated in the pancreatic tissue of rats with AP, as determined by tandem mass spectrometry (TMT) proteomics. This phenomenon was also confirmed in pancreatic acinar cells. To reveal whether S100A11 participates in regulating ferroptosis, an S100A11 knockdown lentivirus was transfected into caerulein\u2010treated pancreatic acinar cells AR42J. Functional results revealed that S100A11 knockdown significantly increased cell viability and GSH levels, while decreasing reactive oxygen species (ROS), lipid ROS, and Fe\n                    <jats:sup>2+<\/jats:sup>\n                    levels in pancreatic acinar cells compared to the control group. In vivo, S100A11 knockdown via adeno\u2010associated virus inhibited caerulein\u2010induced ferroptosis. These findings suggest that S100A11 promotes AP by upregulating ferroptosis, which exacerbates oxidative stress and inflammation in pancreatic tissue.\n                  <\/jats:p>","DOI":"10.1155\/mi\/6971024","type":"journal-article","created":{"date-parts":[[2025,6,13]],"date-time":"2025-06-13T03:34:09Z","timestamp":1749785649000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["S100A11 Promotes Acute Pancreatitis by Upregulating Acinar Cell 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