声带损伤引起固有层细胞外基质无序沉积，进而形成纤维化瘢痕，引起不可逆性发声障碍。如何减缓或逆转声带损伤后过度纤维化的进程是治疗的关键。我们前期研究发现，声带损伤后成纤维细胞增生极度活跃，以胶原为主的细胞外基质紊乱沉积；同时还发现TGF-β1/Smad信号通路参与调控声带修复及纤维化进程，Smad3可能是干预的关键靶点。因此，我们推测TGF-β1/Smad3信号通路可能在声带损伤后纤维化过程中起关键作用，通过microRNA调控该信号通路，有可能抑制或改变声带纤维化过程中成纤维细胞的过度激活及细胞外基质的异常分泌。为此我们拟建立损伤声带microRNA表达谱，筛选与该信号通路相关microRNA，研究其对声带成纤维细胞及细胞外基质的调控作用；同时利用基因转染过表达或敲减此种microRNA，探讨其在损伤声带纤维化进程中可能的作用机制，为探索声带损伤后纤维化的关键干预位点提供依据。

Vocal fold injury often resulted in extracellular matrix disorderly deposition,and thus the fibrous scar formation, which caused irreversible dysphonia. How to slow or reverse the process of excessive fibrosis after vocal fold injury is the key to the treatment. In our previous study, we found that the fibroblasts are extremely hyperplastic, collagen-predominant extracellular matrix disorderly deposition and fibrous tissue hyperplasia after vocal fold injury. Our further study showed that the TGF-β1/Smad3 signaling pathway play an important role in the process of vocal fold fibroblasts over-activities and extracellular matrix abnormal secretion. However, how to regulate this signaling pathway in order to inhibit the process of excessive fibrosis need further study. For this purpose, we plan to set up the microRNA expression profile of vocal fold injury and to investigate the related microRNA of TGF-β1/Smad3 signaling pathway to study its regulation of vocal fold fibroblasts and extracellular matrix in vitro. Meanwhile, we design to construct microR-target smad3-GFP-overexpression lentivirus vector,and implant into the vocal fold injury site of animal model to explore its possible mechanism in the process of vocal fold fibrosis, to understand its significance for the repair and reconstruction of the vocal fold proper lamina, and provide a key intervention of the site for the visualization of the fibrotic process investigate the related microRNA of TGF-β1/Smad3 signaling pathway to study its regulation of vocal fold fibroblasts and extracellular matrix in vitro. Meanwhile, we design to construct microR-target smad3-GFP-overexpression lentivirus vector, and implant into the vocal fold injury site of animal model to explore its possible mechanism in the process of vocal fold fibrosis, to understand its significance for the repair and reconstruction of the vocal fold proper lamina, and provide a key intervention of the site for the visualization of the fibrotic process.