ArticleJournal of thoracic disease2026
Crizotinib attenuates bleomycin-induced pulmonary fibrosis via regulating fibroblast activation.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic interstitial lung disease. Crizotinib is an oral tyrosine kinase inhibitor (TKI), which has been widely used in the treatment of non-small cell lung cancer (NSCLC). Previous studies have demonstrated that crizotinib can inhibit downstream signaling pathways of anaplastic lymphoma kinase (ALK) in lung adenocarcinoma mouse, including pSTAT3, pAKT, and pERK, which also play an important role in the development and progression of pulmonary fibrosis. We conducted this study to investigate the antifibrotic efficacy of crizotinib in pulmonary fibrosis Methods: Fibroblasts were stimulated with TGF-β1 and co-treated with crizotinib to evaluate its impact on fibroblast activation markers as well as main related proteins of signal pathways Results: Conclusions: Through suppressing fibroblast proliferation and activation, crizotinib could alleviate pulmonary fibrosis in BLM induced mice. Crizotinib could inhibit the PI3K/AKT/mTOR, STAT3 and ERK signaling pathways. Crizotinib might be an emerging medication choice for patients with IPF.
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