Abstract
Radiation-induced pulmonary fibrosis (RIPF) is a common consequence of radiation for thoracic tumors, and is accompanied by gradual and irreversible organ failure. This severely reduces the survival rate of cancer patients, due to the serious side effects and lack of clinically effective drugs and methods. Radiation-induced pulmonary fibrosis is a dynamic process involving many complicated and varied mechanisms, of which alveolar type II epithelial (AT2) cells are one of the primary target cells, and the epithelial–mesenchymal transition (EMT) of AT2 cells is very relevant in the clinical search for effective targets. Therefore, this review summarizes several important signaling pathways that can induce EMT in AT2 cells, and searches for molecular targets with potential effects on RIPF among them, in order to provide effective therapeutic tools for the clinical prevention and treatment of RIPF.
Funder
the National Natural Science Foundation of China
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
Reference116 articles.
1. Jin, H., Yoo, Y., Kim, Y., Kim, Y., Cho, J., and Lee, Y.S. (2020). Radiation-Induced Lung Fibrosis: Preclinical Animal Models and Therapeutic Strategies. Cancers, 12.
2. Molecular mechanisms and treatment of radiation-induced lung fibrosis;Ding;Curr. Drug Targets,2013
3. Advances in Molecular Mechanisms and Treatment of Radiation-Induced Pulmonary Fibrosis;Chen;Transl. Oncol.,2019
4. Cellular senescence and radiation-induced pulmonary fibrosis;He;Transl. Res.,2019
5. Scarred Lung. An Update on Radiation-Induced Pulmonary Fibrosis;Jarzebska;Front. Med.,2020
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