线粒体融合与裂解的动力平衡参与心肌缺血再灌注损伤(IRI)的发生与进展。基于Hes1反向调控PTEN，Notch1抑制Pink1、Mfn2、Parkin表达，调节心肌线粒体自噬及融合/裂解的前期发现，我们假设Notch1通过Hes1抑制PTEN表达，阻碍Pink1/Mfn2/Parkin信号转导，纠正线粒体动力失衡，减轻心肌IRI。拟用心肌缺氧/复氧损伤模型，探讨Pink1/Mfn2/Parkin信号转导引发线粒体动力失衡在心肌IRI中的作用；阐述Hes1反向调控PTEN，抑制Pink1表达之效应，揭示以PTEN为介导，Notch1抑制Pink1/Mfn2/Parkin转导的机理；根据呼吸传递链及mPTP变化，论述Notch1纠正线粒体动力失衡的机制，明确Notch1抑制Pink1/Mfn2/Parkin信号转导的心肌保护作用；最后在整体动物上比较论证，为改善临床心肌保护策略奠定理论基础。

Mitochondrial fusion and fission dynamics are involved into occurrence and aggravation of myocardial ischemia reperfusion injury (IRI). Based on the earlier research of Hes1 reverse regulating PTEN and Notch1 modulating myocardial mitochondria autophagy and fusion/fission by regulating the PINK1, Mfn2 and Parkin expression in our lab, we hypothesize that Notch1 corrects mitochondrial dynamics imbalance and reduces myocardial IRI through inhibition of Pink1/Mfn2/Parkin signaling transduction via inhibiting the expression of PTEN mediated by Hes1. The myocardial hypoxia/reoxygenation injury model was established to investigate the effect of Pink1/Mfn2/Parkin signal transduction-induced mitochondrial dynamics imbalance on myocardial IRI. The effect of Hes1 inhibiting Pink1 expression by reverse regulation of PTEN would be elaborated, which will contribute to reveal the mechanism of Notch1 inhibition of Pink1/Mfn2/Parkin signal transduction. The Notch1 in correcting mitochondrial dynamics imbalance is to be elucidated in the alteration of respiratory transmission chain and mPTP, which will beneficial to defined the cardioprotection of Notch1 via the inhibition of Pink1/Mfn2/Parkin signal transduction. Finally, we will explore the foundation for the improvement of clinical myocardial protection strategy through the comparison in the whole animal.