控制肝纤维化的进展对于改善慢性肝病预后以及预防肝癌意义重大。缺乏有效的直接抗肝纤维化制剂是临床治疗肝纤维化的难点以及相关研究领域的热点。申请人通过生信分析以及小鼠肝组织和原代肝星状细胞（HSC）表型实验，发现SND1具有抗肝纤维化功能，接受CCl4腹腔注射后，过表达SND1的转基因小鼠肝纤维化程度减轻，同时原代肝星状细胞的增殖、迁移、分泌纤维化相关蛋白（CTGF）及活化相关蛋白（α-SMA）的能力降低。CTGF是Hippo信号的下游基因，14-3-3蛋白在Hippo信号的调控中发挥重要作用，生信分析及质谱结果支持SND1与14-3-3存在相互作用。基于此，申请人提出“SND1参与14-3-3复合体下调Hippo信号及CTGF表达在延缓肝纤维化进程中的机制研究”这一课题，从蛋白质互作影响转录（共激活）因子胞内定位及下游基因转录调控的角度入手，为深入揭示肝纤维化机制，寻找新药靶点提供理论基础。

It is of great significance to control the progress of liver fibrosis for improving the prognosis of chronic liver disease and preventing liver cancer. The lack of effective direct anti-fibrosis agents is the difficulty of clinical treatment of liver fibrosis and the focus of related research fields. The applicant found that SND1 had the function of anti fibrosis through the analysis of bioinformatic and the phenotypic experiment of mouse liver tissue and primary hepatic stellate cells (HSC). After the intraperitoneal injection of CCl4, the degree of liver fibrosis of transgenic mice overexpressing snd1 was reduced, and the ability of primary hepatic stellate cells to proliferate, migrate, secrete CTGF and α - SMA was also reduced. CTGF is the downstream gene of Hippo signal. 14-3-3 protein plays an important role in the regulation of Hippo signal. The results of bioinformatics and mass spectrometry support the interaction between snd1 and 14-3-3. Based on this, the applicant proposed the topic of "the mechanism of snd1 participating in 14-3-3 complex down regulating Hippo signal and CTGF expression in delaying the process of liver fibrosis", starting from the perspective of protein interaction affecting the intracellular localization of transcription (coactivator) factors and downstream gene transcription regulation, to provide a theoretical basis for further revealing the mechanism of liver fibrosis and finding new drug targets.