Liu et al. constructed a mouse model of diabetic cardiomyopathy using si-MALAT1 and found that silencing MALAT1 can reduce the phosphorylation of MST1 and LATS1 in high-glucose-induced cardiac fibroblasts and promote YAP nuclear translocation, thereby reducing the accumulation of inflammation-related factors TNF-α, IL-1β and collagen (type I and type III) under a high-glucose environment, thereby reducing the inflammatory response and myocardial fibrosis. This evidence concerns the gene MALAT1 and diabetic cardiomyopathy.