Objective To explore the correlation between aging and idiopathic pulmonary fibrosis (IPF) and uncover the underlying molecular mechanisms linking the two. Methods IPF models were established using young (2-month-old) and aged (18-month-old) C57BL/6J mice, which were randomly divided into young control group (Ctrl-Y), young model group (IPF-Y), aged control group (Ctrl-A), and aged model group (IPF-A). Histopathological changes were evaluated using HE and Masson staining. Immunohistochemistry was used to detect the expression levels of COL1A1, α-SMA, and FN. SA-β-Gal staining was employed to assess the degree of senescence. Differential genes were screened based on whole transcriptome sequencing, followed by GO functional annotation and KEGG pathway enrichment analysis. The expression of core genes was verified by qRT-PCR. Results The fibrosis score in the IPF-A group was significantly higher than that in the IPF-Y group (P<0.05). Compared to the IPF-Y group, the protein expressions of COL1A1, α-SMA, and FN in the IPF-A group were significantly upregulated by 16 %, 36 %, and 25 %, respectively (all P<0.05), and the SA-β-Gal positive area for senescence was significantly higher than that in the IPF-Y group. Fifty-five senescence-IPF interactive genes were identified, among which Cdkn1a, MMP3, and Pdcd1 were synergistically upregulated in the IPF-A group (P<0.05). KEGG analysis revealed the activation of signaling pathways such as ECM-receptor interaction, Phagosome, Cytokine-cytokine receptor interaction, Efferocytosis, and PI3K-Akt (FDR<0.05). Conclusions Aging promotes the progression of IPF, and IPF can induce lung tissue senescence. The mechanism may be related to ECM remodeling driven by immunosenescence, inflammatory accumulation, and metabolic disorders.