Fig. 2

Dynamics of non-coding RNAs interacting with histone modification in diabetic cardiomyopathy. Complex epigenetic crosstalk contributes to the progress of diabetic cardiomyopathy under the condition of hyperglycemia and hyperlipidemia. lncRNA DACH1 binds to deacetylase SIRT3, accelerating its ubiquitination-dependent degradation. However, lncRNA Hotair interacts with FUS and stabilize SIRT3 indirectly. The transcription of another deacetylase, SIRT1 is regulated by various miRNAs. miR-22, miR34a, and miR195 could bind to the 3’UTR region of sirt1 mRNA. In addition, MALAT recruits EZH which hold the methyltransferase activity, inhibiting miR-22 transcription by reducing H3K27me3. BRD4 as a coactivator of p65 identifies and activates inflammatory genes, playing a crucial role in inflammation and oxidative stress. With the combination of genetic and epigenetic factors, characteristic pathological changes such as hypertrophy, fibrosis, and apoptosis occur in the heart, resulting in diabetic cardiomyopathy ultimately