ArticleJournal of thoracic disease2026
Copanlisib ameliorates pulmonary fibrosis by modulating cellular autophagy through PI3K/Akt/mTORC1 pathway.
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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9 authors.
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Abstract
Background: Idiopathic pulmonary fibrosis (IPF), a progressive fibrotic interstitial lung disease (ILD), has a poor prognosis, and effective drugs, including nintedanib and pirfenidone, are limited. Therefore, developing new drugs for treating pulmonary fibrosis is of the highest priority. The inhibition of cellular autophagy in lung fibroblasts is an important mechanism involved in pulmonary fibrosis, and the PI3K/Akt/mTORC1 pathway is responsible for modulating the level of intracellular autophagy. As a result, copanlisib, a pan-class I PI3K inhibitor, has promise for preventing pulmonary fibrosis by ameliorating cellular autophagy. This study aimed to evaluate the effect and underlying mechanism of copanlisib in pulmonary fibrosis. Methods: In this study, we evaluated the antifibrotic effect of copanlisib by using a mouse model of bleomycin (BLM)-induced pulmonary fibrosis for Results: As a result, copanlisib markedly alleviated BLM-induced collagen deposition and improved pulmonary function and ventilation volume Conclusions: In conclusion, copanlisib is a promising candidate as a treatment for pulmonary fibrosis.
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