{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T13:05:53Z","timestamp":1780578353490,"version":"3.54.1"},"reference-count":41,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,2,28]],"date-time":"2025-02-28T00:00:00Z","timestamp":1740700800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2025,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The initial inflammatory response plays a pivotal role in the development of acute pancreatitis. MiR\u2010146a is believed to play a key role in negatively regulating inflammation and potentially contributes to anti\u2010inflammatory activity in acute pancreatitis, though its mechanism remains largely unexplored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>This study aimed to explore the effects of miR\u2010146a on AP in mice and clarify its regulatory mechanisms in pancreatic inflammation and damage.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Adult male BALB\/C mice were used. Adeno\u2010associated virus (AAV) vectors were used to modulate miR\u2010146a expression in mice via tail vein injection. AP was induced by intraperitoneal injection of caerulein, caerulein\u2009+\u2009LPS, or\n                      <jats:sc>l<\/jats:sc>\n                      \u2010arginine. Histological analysis, immunohistochemistry staining, immunofluorescence staining, measurements of amylase and lipase activities, and qRT\u2010PCR were performed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Overexpression of miR\u2010146a reduced pancreatic damage and inflammation in caerulein\u2010induced AP. It decreased serum amylase and lipase levels, mitigated pathological features such as interstitial edema and inflammatory cell infiltration in the pancreas and lung, and reduced neutrophil infiltration and proinflammatory cytokine expression. MiR\u2010146a attenuated the activation of the NF\u2010\u03baB signaling pathway by inhibiting the degradation of I\u03baB\u03b1 and the expression of phosphorylated\u2010p65 and reducing the nuclear translocation of NF\u2010\u03baB p65. Similar protective effects of miR\u2010146a were observed in AP models induced by\n                      <jats:sc>l<\/jats:sc>\n                      \u2010arginine and caerulein combined with LPS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>MiR\u2010146a alleviates acute pancreatitis in mice by targeting TRAF6 and suppressing the activation of the NF\u2010\u03baB signaling pathway. These findings suggest that miR\u2010146a could be a potential therapeutic target for AP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/iid3.70163","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T11:04:41Z","timestamp":1741691081000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["MiR\u2010146a Reduces Inflammation in Experimental Pancreatitis via the TRAF6\u2013NF\u2010\u03baB Signaling Pathway in Mice"],"prefix":"10.1002","volume":"13","author":[{"given":"Xiaoyu","family":"Yang","sequence":"first","affiliation":[{"name":"Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuping","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueyang","family":"Li","sequence":"additional","affiliation":[{"name":"Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Xia","sequence":"additional","affiliation":[{"name":"Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-6587-3770","authenticated-orcid":false,"given":"Jianhua","family":"Wan","sequence":"additional","affiliation":[{"name":"Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang Jiangxi 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