{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T02:50:58Z","timestamp":1761101458249,"version":"3.37.3"},"reference-count":57,"publisher":"Wiley","license":[{"start":{"date-parts":[[2021,12,29]],"date-time":"2021-12-29T00:00:00Z","timestamp":1640736000000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012226","name":"Fundamental Research Funds for the Central Universities","doi-asserted-by":"publisher","award":["2042020kf0085"],"award-info":[{"award-number":["2042020kf0085"]}],"id":[{"id":"10.13039\/501100012226","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Analytical Cellular Pathology"],"published-print":{"date-parts":[[2021,12,29]]},"abstract":"<jats:p>Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide and can develop to nonalcoholic steatohepatitis and later hepatic cirrhosis with a high prevalence to hepatocellular carcinoma. Oxidative stress and chronic hepatic inflammation are implicated in the pathogenesis of NAFLD. MicroRNA-137-3p (miR-137-3p) are associated with oxidative stress and inflammation; however, its role and mechanism in NAFLD remain unclear. Mice were fed with a high-fat diet (HFD) for 24 weeks to establish the NAFLD model. To overexpress or suppress hepatic miR-137-3p expression, mice were intraperitoneally injected with the agomir, antagomir, or respective controls of miR-137-3p at a dose of 100\u2009mg\/kg weekly for 6 consecutive weeks before the mice were sacrificed. To validate the involvement of AMP-activated protein kinase alpha (AMPK\u03b1) or cAMP-specific phosphodiesterase 4D (PDE4D), HFD mice were intraperitoneally injected with 20\u2009mg\/kg compound C or 0.5\u2009mg\/kg rolipram every other day for 8 consecutive weeks before the mice were sacrificed. Hepatic miR-137-3p expression was significantly decreased in mice upon HFD stimulation. miR-137-3p agomir alleviated, while miR-137-3p antagomir facilitated HFD-induced oxidative stress, inflammation, and hepatic dysfunction in mice. Mechanistically, we revealed that miR-137-3p is directly bound to the 3<jats:inline-formula>\n                     <a:math xmlns:a=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\">\n                        <a:msup>\n                           <a:mrow\/>\n                           <a:mrow>\n                              <a:mo>\u2032<\/a:mo>\n                           <\/a:mrow>\n                        <\/a:msup>\n                     <\/a:math>\n                  <\/jats:inline-formula>-untranslated region of PDE4D and subsequently increased hepatic cAMP level and protein kinase A activity, thereby activating the downstream AMPK\u03b1 pathway. In summary, miR-137-3p improves NAFLD through activating AMPK\u03b1 and it is a promising therapeutic candidate to treat NAFLD.<\/jats:p>","DOI":"10.1155\/2021\/4853355","type":"journal-article","created":{"date-parts":[[2021,12,30]],"date-time":"2021-12-30T02:05:31Z","timestamp":1640829931000},"page":"1-13","source":"Crossref","is-referenced-by-count":4,"title":["MicroRNA-137-3p Improves Nonalcoholic Fatty Liver Disease through Activating AMPK\u03b1"],"prefix":"10.1155","volume":"2021","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0924-0882","authenticated-orcid":true,"given":"Yuanjie","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, China"},{"name":"Hubei Key Laboratory of Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, 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