在总结前人与自身工作基础上，我们假设：心肌细胞遭受缺氧/复氧损伤刺激时，14-3-3η/HSF5表达同步上调且相互作用，入核启动下游HSPB7表达，发挥心肌保护作用。拟将14-3-3η/HSF5/HSPB7有机结合，用基因转染、RNAi技术确认HSF5保护作用，Co-IP、GST-pull down、酵母双杂交法证实14-3-3η/HSF5间相互作用；胞浆、胞核蛋白分离，Western blot检测14-3-3η/HSF5表达，多荧光标记/DAPI染色/Confocal测14-3-3η/HSF5细胞内之亚定位；用基因转染、RNAi法探讨下游蛋白HSPB7作用；用多荧光标记/Confocal法初步探讨14-3-3η/HSPB7细胞内之亚定位，最后在整体动物实验上比较论证。这将有助于深入了解心肌缺血/再灌注机制，丰富相关知识和理论，阐明新的药物作用靶点，为相应药物研发奠定良好的理论与实验基础。

On the basis of previous studies, We hypothesized that the 14-3-3η/HSF5 expression is up-regulated and interacted，and imported into the nucleus to activate of HSPB7 in the downstream ,and to induce myocardium protection. The aim of this study is to investigate the role of 14-3-3η/HSF5/HSPS in the pathogenesis of acute myocardial injury in a new way. HSF5 protection was confirmed by gene transfection and RNAi. Co-IP, GST-pull down and yeast two-hybrid method were used to confirm the interaction between 14-3-3η/HSF5. The expression of 14-3-3η/HSF5 was detected by cytoplasmic/nuclear protein separation and Western blot analysis. Subcellular localization of 14-3-3η/HSF5 was detected by multi-fluorescent labeling/DAPI/Confocal assay. The effect of downstream effector HSPB7 was investigated by RNAi method. Subcellular localization in 14-3-3η/HSPB7 cells was preliminarily studied by multi-fluorescent labeling/Confocal method. Finally compare and comfirm the results through whole animal experiment. This project will help people to understand the myocardial ischemia/reperfusion phenomenon and its mechanism thoroughly and comprehensively, to further improve and enrich the relevant knowledge and theory, to elucidate possible targets for new drug effects, to lay a good theoretical and experimental basis for the development of myocardial protection drugs.