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Methyltransferase-like 14 (METTL14) emerges as a writer of N6-methyladenosine (m6A) modification. This study was conducted to decipher the role of METTL14 in H\/R-induced cardiomyocyte ferroptosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Mouse cardiomyocytes HL-1 were cultured and underwent H\/R treatment. The degree of ferroptosis after H\/R treatment was appraised by the cell counting kit-8 assay, assay kits (ROS\/GSH\/Fe<jats:sup>2+<\/jats:sup>), and Western blotting (GPX4\/ACSL4). The intracellular expressions of METTL14, pri-miR-146a-5p, miR-146a-5p, or adaptor protein phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) were examined by real-time quantitative polymerase chain reaction or Western blotting, with m6A quantification analysis and RNA immunoprecipitation to determine the total m6A level and the expression of pri-miR-146a-5p bound to DiGeorge critical region 8 (DGCR8) and m<jats:sup>6<\/jats:sup>A-modified pri-miR-146a-5p. The binding of miR-146a-5p to APPL1 was testified by the dual-luciferase assay.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>H\/R treatment induced cardiomyocyte ferroptosis (increased ROS, Fe<jats:sup>2+<\/jats:sup>, and ACSL4 and decreased GSH and GPX4) and upregulated METTL14 expression. METTL14 knockdown attenuated H\/R-induced cardiomyocyte ferroptosis. METTL14 induced the recognition of pri-miR-146a-5p by DGCR8 by increasing m<jats:sup>6<\/jats:sup>A modification on pri-miR-146a-5p, which promoted the conversion of pri-miR-146a-5p into miR-146a-5p and further repressed APPL1 transcription. miR-146a-5p upregulation or APPL1 downregulation limited the inhibitory effect of METTL14 downregulation on H\/R-induced cardiomyocyte ferroptosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>METTL14 promoted miR-146a-5p expression through the recognition and processing of pri-miR-146a-5p by DGCR8, which repressed APPL1 transcription and triggered H\/R-induced cardiomyocyte ferroptosis.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13019-024-02711-0","type":"journal-article","created":{"date-parts":[[2024,4,25]],"date-time":"2024-04-25T10:01:37Z","timestamp":1714039297000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["METTL14-mediated N6-methyladenosine modification induces the ferroptosis of hypoxia\/reoxygenation-induced cardiomyocytes"],"prefix":"10.1186","volume":"19","author":[{"given":"Chunyu","family":"Zhao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianing","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,4,25]]},"reference":[{"issue":"6","key":"2711_CR1","doi-asserted-by":"publisher","first-page":"100299","DOI":"10.1016\/j.xcrm.2021.100299","volume":"2","author":"KN Samman","year":"2021","unstructured":"Samman KN, Mehanna P, Takla E, Grenier JC, Chan MY, Lopes RD, Neely ML, Wang TY, Newby LK, Becker RC, Lordkipanidze M, Ruiz M, Hussin JG, Jolicoeur EM. 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