Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic and fatal interstitial lung disease. The etiology of IPF remains to be fully elucidated and its prognosis remains poor with a short survival period. Solute carrier family 7 member 5 (SLC7A5) is an amino acid transporter that is responsible for the transportation of large neutral amino acids. The expression of SLC7A5 was found to be significantly upregulated in patients with IPF, as well as in the lung tissues of mice with bleomycin (BLM)‑induced pulmonary fibrosis and in human lung fibroblasts induced by transforming growth factor‑β1 (TGF‑β1). Both SLC7A5 knockdown and the use of the selective SLC7A5 inhibitor JPH203 affected the function of TGF‑β1‑induced myofibroblasts by inhibiting the PI3K/AKT/mTOR pathway. In vivo, JPH203 improved BLM‑induced pulmonary fibrosis in mice by inhibiting the activation of the PI3K/AKT/mTOR signaling pathway. Therefore, SLC7A5 may represent a new therapeutic target for IPF. Future research should focus on therapeutic strategies regulating this target for translation into potential effective treatments for IPF in clinical practice.