{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T19:46:33Z","timestamp":1787600793936,"version":"build-2736575974"},"reference-count":28,"publisher":"Cambridge University Press (CUP)","issue":"7","license":[{"start":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T00:00:00Z","timestamp":1709856000000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":["cambridge.org"],"crossmark-restriction":true},"short-container-title":["Cardiol Young"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec id=\"S1047951124000155_as1\"><jats:title>Objective:<\/jats:title><jats:p>Cardiac hypertrophy, acting as a pathologic process of chronic hypertension and coronary disease, and its underlying mechanisms still need to be explored. Long non-coding RNA (LncRNA) potassium voltage-gated channel subfamily Q member 1 Transcript 1 (KCNQ1OT1) has been implicated in myocardial infarction. However, its role in cardiac hypertrophy remains reported.<\/jats:p><\/jats:sec><jats:sec id=\"S1047951124000155_as2\"><jats:title>Method:<\/jats:title><jats:p>To explore the regulated effect of lncRNAKCNQ1OT1 and miR-301b in cardiac hypertrophy, gain-and-lose function assays were tested. The expression of lncRNAKCNQ1OT1 and miR-301b were tested by quantitative real time polymerase chain reaction (qRT-PCR). The levels of transcription factor 7 (Tcf7), Proto-oncogene c-myc (c-myc), Brainnatriureticpeptide (BNP)\u00a0and \u03b2-myosin heavy chain (\u03b2-MHC) were detected by Western blot. Additionally, luciferase analysis revealed interaction between lncRNAKCNQ1OT1, BNP\u03b2-MHCmiR-301b, and Tcf7.<\/jats:p><\/jats:sec><jats:sec id=\"S1047951124000155_as3\"><jats:title>Result:<\/jats:title><jats:p>LncRNAKCNQ1OT1 overexpression significantly induced cardiac hypertrophy. Furthermore, lncRNAKCNQ1OT1 acts as a sponge for microRNA-301b, which exhibited lower expression in cardiac hypertrophy model, indicating an anti-hypertrophic role. Furthermore, the BNP and \u03b2-MHC expression increased, as well as cardiomyocyte surface area, with Ang II treatment, while the effect was repealed by miR-301b. Moreover, the protein expression of Tcf7 was inversely regulated by miR-301b and Antisense miRNA oligonucleotides (AMO)-301b.<\/jats:p><\/jats:sec><jats:sec id=\"S1047951124000155_as4\"><jats:title>Conclusion:<\/jats:title><jats:p>Our study has shown that overexpression of lncRNAKCNQ1OT1 could promote the development of cardiac hypertrophy by regulating miR-301b and Tcf7. Therefore, inhibition of lncRNAKCNQ1OT1 might be a potential therapeutic strategy for cardiac hypertrophy.<\/jats:p><\/jats:sec>","DOI":"10.1017\/s1047951124000155","type":"journal-article","created":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T09:58:49Z","timestamp":1709891929000},"page":"1493-1505","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":3,"title":["The role of lncRNAKCNQ1OT1\/miR-301b\/Tcf7 axis in cardiac 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