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Emerging evidence have implicated long noncoding RNAs (lncRNAs) play a multifaceted role in the progression of cardiac hypertrophy and HF. Here, it is identified that a lncRNA forkhead box O6, opposite strand (Foxo6os) is significantly downregulated in murine HF model induced using transverse aortic constriction (TAC). Knockdown of Foxo6os accelerates cardiomyocyte hypertrophy, reflects as elevated expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and myosin heavy chain 7 (MYH7). Conversely, Foxo6os overexpression can improve cardiac function and alleviate adverse cardiac remodeling. Mechanistically, Foxo6os directly interacts with myosin\u2010binding protein\u2010C (MYBPC3), which then recruits protein kinase C alpha (PKC\u2010\u03b1) to facilitate MYBPC3 phosphorylation, resulting in maintaining myocardial contractility and postponing HF progression. Therefore, these findings underscore the critical role of Foxo6os in preserving cardiomyocyte contractile function, suggesting a potential for Foxo6os as a novel therapeutic target of HF.<\/jats:p>","DOI":"10.1002\/advs.202507365","type":"journal-article","created":{"date-parts":[[2025,6,23]],"date-time":"2025-06-23T10:41:19Z","timestamp":1750675279000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["LncRNA Foxo6os as a Novel \u201c Scaffold\u201d Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure"],"prefix":"10.1002","volume":"12","author":[{"given":"Jie","family":"Sheng","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cardiology and Medical Innovation Center, Shanghai East Hospital, School of Medicine Tongji University  Shanghai 200120 China"},{"name":"Shanghai Arrhythmias Research Center Shanghai East Hospital Tongji University School of Medicine  Shanghai 200120 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