Expression data from healthy and diastolic heart failure rats

Heart failure (HF) with preserved ejection fraction (HFpEF) is rising, whose morbidity, mortality and healthcare costs are similar to HF with reduced ejection fraction (HFrEF). Although substantial molecular pathways lead to the changes in organ and tissue levels, there are still lack of successful treatments for HFpEF given the complexity molecular networks remaining unknown. Here we report that the significantly changed genes of HFpEF rats associates positively with inflammatory processes and immune responses while negatively with calcium ion transport into cytosol. GSEA analysis shows several KEGG pathways are significantly enriched in HFpEF rats including p53 signaling pathway, Toll like receptor signaling pathway and so on. Our study provides new insights into HFpEF pathogenesis and a new therapeutic against HFpEF.射血分数保留型心力衰竭（Heart failure with preserved ejection fraction, HFpEF）的发病率逐年攀升，其发病率、死亡率及医疗成本均与射血分数降低型心力衰竭（Heart failure with reduced ejection fraction, HFrEF）相当。尽管已有诸多分子通路参与器官与组织水平的病理改变，但由于其复杂的分子网络尚未完全阐明，目前仍缺乏针对HFpEF的有效治疗手段。本研究发现，HFpEF模型大鼠的显著差异表达基因与炎症过程及免疫应答呈正相关，而与钙离子向胞质的转运呈负相关。基因集富集分析（Gene Set Enrichment Analysis, GSEA）结果显示，HFpEF模型大鼠体内存在多个显著富集的京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes, KEGG）通路，包括p53信号通路、Toll样受体信号通路等。本研究为HFpEF的发病机制提供了新的见解，并为其治疗提供了全新的研究方向。