与呼吸系统疾病相关的低氧性肺动脉高压的主要病理学特点为低氧性肺血管重构，其机制研究主要集中在生长因子、血管张力调节递质、离子通道、基因突变等方面，而其炎性机制仍有待阐明。近年来，促炎因子IL-17被认为与血管性疾病有关。我们前期研究发现wnt/beta-catenin信号通路的活化参与低氧诱导的肺动脉平滑肌细胞的增殖，IL-17信号通路与wnt/beta-catenin信号通路又存在着“串话”。由此我们假设低氧影响IL-17的分泌，IL-17可通过其下游相关信号通路及其与wnt/beta-catenin信号通路间的“串话”参与低氧性肺血管重构的形成。基于此，本研究拟采用体外细胞培养以及低氧性肺动脉高压动物模型等手段，运用流式细胞术、qRT-PCR、Western blot、基因沉默及过表达等方法，探究IL-17在低氧性肺血管重构形成中的作用及其机制，从而为疾病治疗提供新的理论依据。

Hypoxic pulmonary artery hypertension (HPH) is related with many pulmonary diseases, whose main pathological characteristic is hypoxic pulmonary vascular remodeling. Its pathogenesis is focused on growth factors, vascular tone mediators, ions, and gene mutation et al., but the inflammatory mechanisms are largely unknown. Pro-inflammatory cytokine IL-17 has become an international hotspot, and its role in vascular disease attracts attention gradually. We have reported that wnt/beta-catenin signal was activated in the hypoxia-induced pulmonary artery smooth muscle cells’ proliferation, and IL-17 signal has cross-talk with wnt/beta-catenin signal, then we propose the hypothesis that hypoxia can induce the secretion of IL-17, IL-17 participates the pulmonary vascular remodeling via its cross-talk with wnt/beta-catenin signal. This study is designed to research the role of IL-17 in hypoxic pulmonary vascular remodeling and its possible mechanisms both in vivo and in vitro, using flow cytometry, qRT-PCR, Western blot, siRNA and gene overexpression. We try to provide new theoretical basis for treatment of HPH.