转化生长因子(transforming growth factor, TGF)-β1是已知最强的致纤维化细胞因子，阻断TGF-β1经典和非经典信号通路均可有效阻止肺纤维化病理进程。然而，鉴于TGF- β1经典信号通路在机体正常功能维持中的重要作用，有必要探讨TGF-β非经典通路活化的分子机制。我们课题组前期的研究表明，胶原受体DDR2促肺纤维化病理进程与其能够特异性地协同TGF-β非经典通路的活化相关，提示靶向DDR2有可能成为选择性抑制TGF-β非经典通路的关键分子靶点。本项目旨在深入研究这种协同作用的分子模式，从而为研发副作用更小的治疗策略用于肺纤维化的治疗提供理论依据。

Transforming growth factor ( TGF)-β1 is the most potent pro-fibrotic cytokine. Blockade of both canocial and non-canocial TGF-β1 signaling can prevent the development of pulmonary fibrosis (PF). However, in view of the important roles of canocial TGF-β1 pathway in the maintenance of normal function, it is necessary to explore the mechanisms underlying the activation of non-canocial TGF-β1 signaling. The data from our lab demonstrated that collagen receptor DDR2 could promote the pathogenesis of PF partially through regulating the activation of non-canocial TGF-β1 cascade. Thus, the current project aims to investigate how DDR2 affects TGF-β1 pathway so as to develop or design therapeutic strategies for the treatment of PF with less side effect.