Therefore, we investigated the role of telomere damage-mediated senescence in alveolar epithelial type II (AEII) cells and macrophages in injury and inflammation of lipopolysaccharide (LPS)-induced ALI in mice.Cell type-specific deletion of Trf1 (telomeric repeat-binding factor 1) was achieved using tamoxifen-inducible Cre-loxP mouse models driven by the Sftpc (surfactant protein c) promoter for AEII cells or Lyz2 (lysozyme 2) promoter for macrophages to induce telomere damage in respective cell types. The gene discussed is SFTPC; the disease is acute respiratory distress syndrome.