Senescent cells are strongly implicated in various diseases including idiopathic pulmonary fibrosis. In our previous study, we confirmed expression of p16, a key marker of cellular senescence, in the alveolar epithelial cells (AECs) of lungs from bleomycin-induced pulmonary fibrosis model mice. Although AECs have been reported to contribute to lung fibrosis through epithelial-mesenchymal transition (EMT), it remains unclear whether the induction of EMT is influenced by AEC senescence. In the present study, we investigated the roles of AEC senescence in lung fibrosis using AEC-specific p16 knockout (cKO) mice. Intraperitoneal administration of bleomycin caused pulmonary fibrosis in both control and cKO mice. However, the amount of soluble collagen in bronchoalveolar lavage fluid and collagen deposition in lung tissue, indicators of lung fibrosis, were lower in cKO compared with control group. Furthermore, the mRNA expression of Col1a1, which promotes lung fibrosis, tended to be decreased in the lungs of cKO mice compared with controls. In addition, the expression of EMT marker genes (Cdh2 and Vim) also tended to be lower in the lungs of cKO mice. These results suggest that cellular senescence mediated by p16 expression in AEC contributes to progression of lung fibrosis.