{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T15:22:03Z","timestamp":1780500123741,"version":"3.54.1"},"reference-count":25,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T00:00:00Z","timestamp":1721779200000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,7,1]],"date-time":"2024-07-01T00:00:00Z","timestamp":1719792000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Heart failure (HF) prognosis depends on various regulatory factors; microRNA\u2010128 (miR\u2010128) is identified as a regulator of cardiac fibrosis, contributing to HF. MyoD family inhibitor (MDFI), which is reported to be related with Wnt\/\u03b2\u2010catenin pathway, is supposed to be regulated by miR\u2010128. This study investigates the interaction between miR\u2010128 and MDFI in cardiomyocyte development and elucidates its role in heart injury. Gene expression profiling assessed miR\u2010128's effect on MDFI expression in HF using qPCR and Western blot analysis. Luciferase assays studied the direct interaction between miR\u2010128 and MDFI. MTT, transwell, and immunohistochemistry evaluated the effects of miR\u2010128 and MDFI on myocardial cells in mice HF. Genescan and luciferase assays validated the interaction between miR\u2010128 and MDFI sequences. miR\u2010128 mimics significantly reduced MDFI expression at mRNA and protein levels with decrease rate of 55%. Overexpression of miR\u2010128 promoted apoptosis with the increase rate 65% and attenuated cardiomyocyte proliferation, while MDFI upregulation significantly enhanced proliferation. Elevated miR\u2010128 levels upregulated Wnt1 and \u03b2\u2010catenin expression, whereas increased MDFI levels inhibited these expressions. Histological analysis with haematoxylin and eosin staining revealed that miR\u2010128 absorption reduced MDFI expression, hindering cell proliferation and cardiac repair, with echocardiography showing corresponding improvements in cardiac function. Our findings suggest miR\u2010128 interacts with MDFI, playing a crucial role in HF management by modulating the Wnt1\/\u03b2\u2010catenin pathway. Suppression of miR\u2010128 could promote cardiomyocyte proliferation, highlighting the potential value of the miR\u2010128\/MDFI interplay in HF treatment.<\/jats:p>","DOI":"10.1111\/jcmm.18546","type":"journal-article","created":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T11:23:17Z","timestamp":1721820197000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The role of\n                    <scp>miR<\/scp>\n                    \u2010128 and\n                    <scp>MDFI<\/scp>\n                    in cardiac hypertrophy and heart failure: Mechanistic"],"prefix":"10.1111","volume":"28","author":[{"given":"Sun","family":"Yanjun","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Surgery Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-1212-9131","authenticated-orcid":false,"given":"Gu","family":"Yunfen","sequence":"additional","affiliation":[{"name":"Department of Intensive care unit, Ruijin Hospital Shanghai Jiaotong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao","family":"Haoyi","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wang","family":"Zhe","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-0820-3699","authenticated-orcid":false,"given":"Qiu","family":"Jiapei","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Surgery Ruijin Hospital, Shanghai Jiao Tong University School of Medicine  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,7,24]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.15420\/cfr.2016:25:2"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/ehf2.12005"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2006.07.007"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41569-018-0007-y"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1186\/s10020-020-00242-7"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2017.00775"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms15870"},{"key":"e_1_2_9_9_1","doi-asserted-by":"publisher","DOI":"10.1080\/15476278.2021.2020018"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110.169391"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.01180-14"},{"key":"e_1_2_9_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/bies.950170306"},{"key":"e_1_2_9_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80148-8"},{"key":"e_1_2_9_14_1","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.605875"},{"key":"e_1_2_9_15_1","doi-asserted-by":"publisher","DOI":"10.1159\/000489595"},{"key":"e_1_2_9_16_1","unstructured":"WangJ LiuV LiuVW.ERK5 as a Metabolic Regulator in the Heart. 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