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In this study, we aimed to systematically profile global RNA N6-methyladenosine (m 6 A) modification patterns in a mouse model of diabetic cardiomyopathy (DCM). Patterns of m 6 A in DCM and normal hearts were analyzed via m 6 A-specific methylated RNA immunoprecipitation followed by high-throughput sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). m 6 A-related mRNAs were validated by quantitative real-time PCR analysis of input and m 6 A immunoprecipitated RNA samples from DCM and normal hearts. A total of 973 new m 6 A peaks were detected in DCM samples and 984 differentially methylated sites were selected for further study, including 295 hypermethylated and 689 hypomethylated m 6 A sites (fold change (FC) > 1.5,  P  < 0.05). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway analyses indicated that unique m 6 A-modified transcripts in DCM were closely linked to cardiac fibrosis, myocardial hypertrophy, and myocardial energy metabolism. Total m 6 A levels were higher in DCM, while levels of the fat mass and obesity-associated (FTO) protein were downregulated. Overexpression of FTO in DCM model mice improved cardiac function by reducing myocardial fibrosis and myocyte hypertrophy. Overall, m 6 A modification patterns were altered in DCM, and modification of epitranscriptomic processes, such as m 6 A, is a potentially interesting therapeutic approach.

Changes in N6-Methyladenosine Modification Modulate Diabetic Cardiomyopathy by Reducing Myocardial Fibrosis and Myocyte Hypertrophy