Copanlisib ameliorates pulmonary fibrosis by modulating cellular autophagy through PI3K/Akt/mTORC1 pathway

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.