ACTA1 and pulmonary fibrosis: These block the NF-κB signaling cascade, significantly downregulate pro-inflammatory mediators such as TNF-α, IL-6, IL-1β, and MMP-12, and reduce neutrophil and macrophage count infiltration; inhibit TGF-β1-driven epithelium-mesenchymal transition (EMT), reverse E-cadherin downregulation, and reduce α-SMA, COL1A1, and Fibronectin expression, thereby alleviating the pulmonary fibrosis process; meanwhile, upregulate cilia-related genes such as Ttc21a and Cfap45, and repair airway epithelium cilia structure and motor function.