biostudies-literatureYang YShenyang Science and Technology Bureau (Science and Technology Bureau of Shenyang)National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint FundNational Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund)National Natural Science Foundation of ChinaShenyang Science and Technology BureauNational Natural Science Foundation of China (National Science Foundation of China)167https://www.ebi.ac.uk/biostudies/studies/S-EPMC8983679biostudies-literatureUnknown8(1)Pathological cardiac hypertrophy is a key contributor in heart failure (HF). Long non-coding RNAs (lncRNAs) and N⁶-methyladenosine (m⁶A) modification play a vital role in cardiac hypertrophy respectively. Nevertheless, the interaction between lncRNA and m⁶A methylase in cardiac hypertrophy is scarcely reported. Here, we constructed a cardiac hypertrophy mouse model by transverse aortic constriction (TAC) surgery and H9c2 cell model by stimulating with AngII. We found that lncRNA MIAT mRNA level, and m⁶A RNA methylation reading protein Ythdf2 mRNA and protein levels, were significantly increased in the cardiac hypertrophy model both in vivo and vitro. MIAT or Ythdf2 overexpression aggravated cardiac hypertrophy, and vice versa. Through bioinformatCell death discoveryThe lncRNA MIAT regulates CPT-1a mediated cardiac hypertrophy through m⁶A RNA methylation reading protein Ythdf2.PMC898367919-112-4-0038197021725Mbikyo MBYang YLi ZZhang JZhang YZhang NfalseThe lncRNA MIAT regulates CPT-1a mediated cardiac hypertrophy through m⁶A RNA methylation reading protein Ythdf2.Pathological cardiac hypertrophy is a key contributor in heart failure (HF). Long non-coding RNAs (lncRNAs) and N⁶-methyladenosine (m⁶A) modification play a vital role in cardiac hypertrophy respectively. Nevertheless, the interaction between lncRNA and m⁶A methylase in cardiac hypertrophy is scarcely reported. Here, we constructed a cardiac hypertrophy mouse model by transverse aortic constriction (TAC) surgery and H9c2 cell model by stimulating with AngII. We found that lncRNA MIAT mRNA level, and m⁶A RNA methylation reading protein Ythdf2 mRNA and protein levels, were significantly increased in the cardiac hypertrophy model both in vivo and vitro. MIAT or Ythdf2 overexpression aggravated cardiac hypertrophy, and vice versa. Through bioinformat2022-01-01T00:00:00Z2022 Apr2025-04-21T16:51:51.962Z2025-04-21T16:51:51.962ZS-EPMC89836793538315210.1038/s41420-022-00977-8