{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T19:03:34Z","timestamp":1769972614026,"version":"3.49.0"},"reference-count":54,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T00:00:00Z","timestamp":1663286400000},"content-version":"vor","delay-in-days":258,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Key Research Project of Hebei Provincial Health Commission","award":["20210514"],"award-info":[{"award-number":["20210514"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>. DCM is the most common and malignant complication of diabetes. It is characterized by myocardial dilatation, hypertrophy, fibrosis, ventricular remodeling, and contractile dysfunction. Although many studies have demonstrated the function of miRNAs in the progression of DCM, but the specific role of miR\u2010372\u20103p in DCM remains unknown. <jats:italic>Methods<\/jats:italic>. C57\/BL6J mice were used to construct mouse models of DCM by intraperitoneal injection of STZ (50\u2009mg\/kg\/d) for 5 consecutive days. Then the mice were randomly divided into model group (intramyocardial injection of empty lentivirus) and miR\u2010372\u20103p KD group (intramyocardial injection of miR\u2010372\u20103p KD lentivirus at 10<jats:sup>9<\/jats:sup>\/mouse). Besides, the control group (injection of 0.9% normal saline) was also set up. LY294002, a PI3K inhibitor, was employed in the current study. Western blotting, immunofluorescence staining, quantitative ultrasound method, Masson\u2019s trichrome staining, and bioinformatics analysis were performed. <jats:italic>Results<\/jats:italic>. It was found that miR\u2010372\u20103p KD significantly improved left ventricular dysfunction and cardiac hypertrophy in DCM mice. Furthermore, it also improved myocardial interstitial fibrosis and remodeling in DCM mice. Immunofluorescence staining and RT\u2010qPCR revealed that miR\u2010372\u20103p KD might accelerate cardiac remodeling by increasing angiogenesis in DCM mice. Western blotting results revealed that miR\u2010372\u20103p was an upstream target of the PI3K\/AKT\u2010mTOR and HIF\u20101<jats:italic>\u03b1<\/jats:italic> signals, as well as NOX2, NOX4, which were responsible for angiogenesis in DCM mice. Besides, the <jats:italic>in vitro<\/jats:italic> experiment showed that LY294002 markedly diminished the increased expression levels of p\u2010PI3K, AKT, p\u2010mTOR, p\u2010P70S6K, HIF\u20101<jats:italic>\u03b1<\/jats:italic>, NOX2, and NOX4 in the model group and the miR\u2010372\u20103p KD group, suggesting that PI3K signaling pathway and oxidative stress are involved in miR\u2010372\u20103p KD\u2010induced angiogenesis in HG\u2010stimulated C166 cells. <jats:italic>Conclusions<\/jats:italic>. MiR\u2010372\u20103p KD inhibits the development of DCM <jats:italic>via<\/jats:italic> activating the PI3K\/AKT\/mTOR\/HIF\u20101<jats:italic>\u03b1<\/jats:italic> signaling pathway or suppressing oxidative stress. This offers an applicable biomarker for DCM treatment.<\/jats:p>","DOI":"10.1155\/2022\/4342755","type":"journal-article","created":{"date-parts":[[2022,9,16]],"date-time":"2022-09-16T23:35:07Z","timestamp":1663371307000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["[Retracted] Knockdown of miR\u2010372\u20103p Inhibits the Development of Diabetic Cardiomyopathy by Accelerating Angiogenesis via Activating the PI3K\/AKT\/mTOR\/HIF\u20101\u03b1 Signaling Pathway and Suppressing Oxidative Stress"],"prefix":"10.1155","volume":"2022","author":[{"given":"Zhimin","family":"Han","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Danyang","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mengfan","family":"Han","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rongjin","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3668-7310","authenticated-orcid":false,"given":"Yongmei","family":"Hao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2022,9,16]]},"reference":[{"key":"e_1_2_11_1_2","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2020.00042"},{"key":"e_1_2_11_2_2","doi-asserted-by":"publisher","DOI":"10.2174\/1871530320666200731174724"},{"key":"e_1_2_11_3_2","article-title":"Recent molecular events concerned with pathogenesis and management of diabetic cardiomyopathy","volume":"5","author":"Jadon A. 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