Objective To explore the correlation between aging and idiopathic pulmonary fibrosis (IPF) and reveal the underlying molecular mechanisms. Methods IPF models were established using young (2-month-old) and aged (18-month-old) C57BL / 6J mice by intratracheal instillation of bleomycin (BLM) hydrochloride (2. 5 mg / kg) after fully exposing the trachea. The control groups received an equal volume of saline administered in the same manner. Mice were divided randomly into four groups: a young control (Ctrl-Y)group, young model (IPF-Y) group, aged control ( Ctrl-A) group, and aged model ( IPF-A) group. Histopathological changes were evaluated by hematoxylin-eosin and Masson staining. Collagen type Ⅰ alpha 1 chain (COL1A1), α-smooth muscle actin (SMA),and fibronectin ( FN ) expression were detected by immunohistochemistry. Cell senescence was detected by senescence-associated beta-galactosidase ( SA-β-Gal ) staining. Differentially expressed genes were detected by transcriptome sequencing, followed by gene ontology functional annotation(GO) and kyoto encyclopedia of genes and genomes ( KEGG) pathway enrichment analysis. Core gene expression was validated by quantitative reverse transcription-polymerase chain reaction. Results The fibrosis score was significantly higher in the IPF-A group compared with the IPF-Y group (P<0. 05). Expression levels of α-SMA, and FN were significantly upregulated in the IPF-A group versus the IPF-Y group by 36%, and 25%, respectively (P<0. 05). The SA-β-Gal-positive area indicating senescence was significantly larger in the IPF-A group than 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 extracellular matrix (ECM)-receptor interaction, phagosome, cytokine-cytokine receptor interaction, efferocytosis, and PI3K-Akt (FDR<0. 05). Conclusions aging promotes IPF progression, which induces lung tissue senescence. The underlying mechanism may involve ECM remodeling driven by immunosenescence, inflammatory accumulation, and metabolic disorders.