细胞自噬(autophagy)，又称为Ⅱ型细胞死亡，是细胞在自噬相关基因的调控下利用溶酶体降解自身受损的细胞器和大分子物质的过程。其在烧伤后心肌细胞损伤中发挥重要作用，但机制尚未阐明。我们的前期研究发现Notch-STAT3可通过调控活性氧的生成来达到烧伤后心肌保护作用。文献研究表明：抑制mTOR可以促进自噬，而STAT3是mTOR调节自噬的信号分子。因此我们推测Notch是否可通过STAT3来调控mTOR从而影响烧伤时心肌细胞自噬。为此，我们将通过小鼠烧伤模型，分组予自噬抑制剂及诱导剂、Notch条件剔除与增强，通过分子生物学、免疫化学等技术观察自噬小体，Notch、mTOR及自噬相关蛋白的表达。进一步通过腺病毒激活或干扰关键分子STAT3，观察Notch、mTOR及自噬的变化。明确Notch信号途径对 mTOR及心肌自噬调控的分子机制及调控的关键位点，为治疗烧伤后心肌损伤提供新思路。

Autophagy, also known as programmed cell death (II), is the process by which cells degrade their damaged organelles and macromolecules under the control of autophagy related genes.It plays an important role in the injury of myocardial cells after burn injury, but the mechanism has not been elucidated. Our previous studies have shown that Notch-STAT3 can protect the myocardium after burn by regulating the production of reactive oxygen species(ROS). A number of studies have shown that inhibition of mTOR could promotes autophagy, and STAT3 is a signaling molecule that regulates autophagy by mTOR. Therefore, we hypothesized that Notch could regulate the mTOR by STAT3, which could affect myocardial autophagy after burn.In order to confirm our hypothesis, we will devided burn mice model into several groups, and each group was given autophagy inhibitors or inducers and Notch elimination or enhancement. The expressions of Notch, mTOR and autophagy marker protein were observed by molecular biology, electron microscopy and immunofluorescence staining, etc. Furthermore, the activation of Notch, mTOR and autophagy were observed by molecular biological methods such as adenovirus to activate or interfere with the key molecule STAT3. Our goal is to clarify the molecular mechanism of Notch signaling pathway regulating autophage by mTOR, and to provide a new way for the prevention and treatment of early myocardial injury after burn.