{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T20:58:42Z","timestamp":1773694722048,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,1,27]],"date-time":"2021-01-27T00:00:00Z","timestamp":1611705600000},"content-version":"vor","delay-in-days":26,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012226","name":"Fundamental Research Funds for the Central Universities","doi-asserted-by":"publisher","award":["2042020kf0046"],"award-info":[{"award-number":["2042020kf0046"]}],"id":[{"id":"10.13039\/501100012226","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012226","name":"Fundamental Research Funds for the Central Universities","doi-asserted-by":"publisher","award":["2042019kf0059"],"award-info":[{"award-number":["2042019kf0059"]}],"id":[{"id":"10.13039\/501100012226","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>Doxorubicin (DOX) could trigger congestive heart failure, which largely limited the clinical use of DOX. microRNAs (miRNAs) were closely involved in the pathogenesis of DOX\u2010induced cardiomyopathy. Here, we aimed to investigate the effect of miR\u2010152 on DOX\u2010induced cardiotoxicity in mice. To study this, we used an adeno\u2010associated viral vector to overexpress miR\u2010152 in mice 6 weeks before DOX treatment, using a dose mimicking the concentrations used in the clinics. In response to DOX injection, miR\u2010152 was significantly decreased in murine hearts and cardiomyocytes. After DOX treatment, mice with miR\u2010152 overexpression in the hearts developed less cardiac dysfunction, oxidative stress, inflammation, and myocardial apoptosis. Furthermore, we found that miR\u2010152 overexpression attenuated DOX\u2010related oxidative stress, inflammation, and cell loss in cardiomyocytes, whereas miR\u2010152 knockdown resulted in oxidative stress, inflammation, and cell loss in cardiomyocytes. Mechanistically, this effect of miR\u2010152 was dependent on the activation of nuclear factor (erythroid\u2010derived 2)\u2010like 2 (Nrf2) in response to DOX. Notably, Nrf2 deficiency blocked the protective effects of miR\u2010152 against DOX\u2010related cardiac injury in mice. In conclusion, miR\u2010152 protected against DOX\u2010induced cardiotoxicity via the activation of the Nrf2 signaling pathway. These results suggest that miR\u2010152 may be a promising therapeutic target for the treatment of DOX\u2010induced cardiotoxicity.<\/jats:p>","DOI":"10.1155\/2021\/8860883","type":"journal-article","created":{"date-parts":[[2021,1,28]],"date-time":"2021-01-28T02:50:05Z","timestamp":1611802205000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Activation of Nrf2 by miR\u2010152 Inhibits Doxorubicin\u2010Induced Cardiotoxicity via Attenuation of Oxidative Stress, Inflammation, and Apoptosis"],"prefix":"10.1155","volume":"2021","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2463-6030","authenticated-orcid":false,"given":"Wen-Bin","family":"Zhang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6433-139X","authenticated-orcid":false,"given":"Xin","family":"Lai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3606-8974","authenticated-orcid":false,"given":"Xu-Feng","family":"Guo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2021,1,27]]},"reference":[{"key":"e_1_2_8_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2012.03.006"},{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/cam4.1886"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.21.12610"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2017.10.008"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1080\/01926230490502601"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.21037\/cdt-19-707"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2020.104846"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/jcb.29840"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000146889.46519.27"},{"key":"e_1_2_8_10_2","first-page":"4592","article-title":"Doxorubicin treatment in vivo causes cytochrome C release and cardiomyocyte apoptosis, as well as increased mitochondrial efficiency, superoxide dismutase activity, and Bcl-2:Bax ratio","volume":"62","author":"Childs A. 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