Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression

Myocardial fibrosis is the most common pathological feather of adverse ventricular remodeling, and persistent fibrotic extension decreases myocardial compliance, promotes the development of heart failure. Epigenetics has been considered to play a potent regulatory role in the development of excessive myocardial fibrosis. Although, the explicit mechanism of epigenetic regulation in myocardial fibrosis still needs to be fully elucidated.RNA-seq analysis was used to screen differentially expressed genes in cardiac fibroblasts isolated from KDM5B KO and littermate control WT mice hearts at day 7 after MI operation. Overall design: 8-10-week-old male KDM5B KO mice and their corresponding WT mice were subjected to myocardial infarction by ligation of the left anterior descending coronary artery. At 7 days after myocardial infarction, cardiac fibroblasts were isolated for RNA-seq analysis. Each group contain with 3 replicates