闭塞性细支气管炎（BOS/OB）是制约肺移植后患者生存的主要因素，上皮细胞间质转化（EMT）在BOS的发生发展中发挥重要作用。我们前期研究发现BOS的发生与TGF-β1有关，法尼基二磷酸合酶（FPPS）介导了TGF-β1诱导的EMT进程。另外BOS大鼠肺中细胞自噬的水平更低，增强自噬可以抑制细胞EMT进程，提示自噬可能参与了EMT过程及BOS的发生。同时我们还发现TGF-β1及FPPS也可以调控细胞自噬，表明它们可能通过自噬调控EMT的进程。本研究拟通过对肺移植后合并BOS患者肺组织进行FPPS、自噬标记物和EMT标记物检测，确定FPPS、自噬、EMT之间的关系；采用体外培养人气道上皮细胞，大鼠肺移植BOS模型，探讨FPPS调控的自噬相关EMT在BOS中的作用和分子机制，以期为临床预防和治疗肺移植后BOS提供理论依据和针对性指导。

Bronchiolitis obliterans syndrome or Obliterative bronchiolitis (BOS/OB) is a predominant factor limiting the survival of patients after lung transplantation. Epithelial-mesenchymal transition (EMT) plays an important role in the occurrence and development of BOS. Our previous study showed that the occurrence of BOS was related to TGF-β1, and FPPS mediated TGF-β1-induced EMT. In addition, the level of autophagy in the lungs of BOS rats was lower, and enhanced autophagy inhibited the process of EMT, suggesting that autophagy may be involved in the EMT process and the occurrence of BOS. We also found that TGF-β1 and FPPS could also regulate autophagy, suggesting that they might regulate the progression of EMT through autophagy. In this study, we will determine expression of FPPS, autophagy markers and EMT markers and analyze the correlation expression of FPPS, autophagy markers and EMT markers. Then we will investigate whether FPPS mediates autophagy-associated epithelial-mesenchymal transition in bronchiolitis obliterans syndrome and the underlying molecular mechanism by using human airway epithelial cell lines cultured in vitro and rat lung transplant model with BOS, which may provide theoretical basis and pertinent guidance for clinical prevention and treatment of BOS after lung transplantation.