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Filgotinib Improves Experimental Pulmonary Fibrosis by Modulating JAK1/STAT3/SOCS3/IL‐17A Signalling
Data Availability Statement The original contributions of this study are included in the article/Supplementary Material; further inquiries can be directed to the corresponding authors.
Sapanisertib attenuates pulmonary fibrosis by modulating Wnt5a/mTOR signalling
Abstract Sapanisertib is an orally bioavailable ATP-dependent high-potential raptor-mTOR (TORC1) inhibitor with antineoplastic activity. Here, the impact of sapanisertib was assessed on transforming growth factor-β1 (TGF-β1)-treated L929 and A549 cells and on a rat model of bleomycin pulmonary fibrosis.
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