支气管平滑肌增殖是慢阻肺气道重塑的主要病理改变。前期研究表明，生物燃料PM2.5可导致慢阻肺气道平滑肌层增厚，且长链非编码RNA（LncRNA）参与气道重塑。预实验结果显示：LncRNA LINC00926在慢阻肺患者肺组织高表达，主要定位于人支气管平滑肌细胞核。将LINC00926敲低后，TCF12和Cyclin D1表达下调，从而抑制人支气管平滑肌细胞增殖。TCF参与Wnt/β-Catenin通路激活促进Cyclin D1的转录。因此我们提出LINC00926通过TCF12激活Wnt/β-Catenin/TCF通路从而增强Cyclin D1的转录促进人支气管平滑肌细胞增殖导致气道重塑的科学假说。本研究从细胞和人群两个层面探讨LINC00926通过TCF12调控支气管平滑肌细胞增殖在生物燃料PM2.5致慢阻肺中的作用，为进一步阐明慢阻肺气道重塑机制和寻找新的治疗靶点提供更充分的科学依据。

Cell proliferation of human bronchial smooth muscle cells (HBSMCs) is the main pathological change of airways remodeling in COPD. Our previous studies have shown that biomass fuel PM2.5 exposure can lead to thickening of airway layers in COPD, and long noncoding RNA (LncRNA) is involved in airway remodeling. The pre-experiment showed that: we screened a highly differentially expressed LncRNA LINC00926 from the lung tissues of COPD patients. LINC00926 mainly expressed in the nucleus of HBSMCs. After knocking down of LINC00926, the protein expression of TCF12 and Cyclin D1 were down-regulated, and repressesed cell proliferation of HBSMCs. Therefore, we propose that the scientific hypothesis that LINC00926 via TCF12 to activate the Wnt/β-Catenin/TCF pathway to enhance the transcription of Cyclin D1 causing the cell proliferation of HBSMCs leading to airway remodeling of COPD. This project will elucidate a crucial role of LncRNA LINC00926 regulating TCF12 by promoting HBSMCs proliferation in COPD induced by biomass fuel PM2.5. The data will further elucidate the mechanism of airway remodeling in COPD and seek new therapeutic targets in the treatment of COPD.