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Translational inhibition has been shown to be an effective means of treating cardiac hypertrophy, although system-wide side effects are common. Regulators of translation, such as cardiac-specific long noncoding RNAs (lncRNAs), could provide new, more targeted therapeutic approaches to inhibit cardiac hypertrophy. Therefore, we generated mice lacking a previously identified lncRNA named\n                    <jats:italic>CARDINAL<\/jats:italic>\n                    to examine its cardiac function. We demonstrate that\n                    <jats:italic>CARDINAL<\/jats:italic>\n                    is a cardiac-specific, ribosome-associated lncRNA and show that its expression was induced in the heart upon pathological cardiac hypertrophy and that its deletion in mice exacerbated stress-induced cardiac hypertrophy and augmented protein translation. In contrast, overexpression of\n                    <jats:italic>CARDINAL<\/jats:italic>\n                    attenuated cardiac hypertrophy in vivo and in vitro and suppressed hypertrophy-induced protein translation. Mechanistically,\n                    <jats:italic>CARDINAL<\/jats:italic>\n                    interacted with developmentally regulated GTP-binding protein 1 (DRG1) and blocked its interaction with DRG family regulatory protein 1 (DFRP1); as a result, DRG1 was downregulated, thereby modulating the rate of protein translation in the heart in response to stress. This study provides evidence for the therapeutic potential of targeting cardiac-specific lncRNAs to suppress disease-induced translational changes and to treat cardiac hypertrophy and heart failure.\n                  <\/jats:p>","DOI":"10.1172\/jci169112","type":"journal-article","created":{"date-parts":[[2024,5,14]],"date-time":"2024-05-14T12:00:47Z","timestamp":1715688047000},"source":"Crossref","is-referenced-by-count":26,"title":["The long noncoding RNA CARDINAL attenuates cardiac hypertrophy by modulating protein translation"],"prefix":"10.1172","volume":"134","author":[{"given":"Xin","family":"He","sequence":"first","affiliation":[{"name":"Department of Cardiology, Center for Translational Medicine, Institute of Precision Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China."},{"name":"Department of Cardiology, Boston Children\u2019s Hospital, Harvard Medical School, Boston, Massachusetts, USA."},{"name":"NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, Guangzhou, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiqun","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Center for Translational Medicine, Institute of Precision Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China."},{"name":"NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, Guangzhou, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6200-2974","authenticated-orcid":true,"given":"Yao Wei","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Boston Children\u2019s Hospital, Harvard Medical School, Boston, Massachusetts, USA."},{"name":"Vascular Biology Program, Department of Surgery, Boston Children\u2019s Hospital, Harvard Medical School, Boston, Massachusetts, 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