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

心肌纤维化是不良心室重构最常见的病理特征，持续性纤维化进展会降低心肌顺应性，促进心力衰竭的发生发展。表观遗传学被认为在过度心肌纤维化的发生发展中发挥强效调控作用，但其在心肌纤维化中的确切调控机制仍有待完全阐明。
本研究采用RNA测序（RNA-seq）分析，筛选心肌梗死（Myocardial Infarction, MI）术后7天，从KDM5B敲除（Knockout, KO）小鼠及同窝对照野生型（Wild Type, WT）小鼠心脏中分离的心肌成纤维细胞内的差异表达基因。整体实验设计如下：选取8~10周龄的雄性KDM5B KO小鼠及其对应WT小鼠，通过结扎左前降支冠状动脉构建心肌梗死模型；于心肌梗死后7天分离心肌成纤维细胞进行RNA-seq分析。每组设置3个生物学重复。