@Article{biocell.2022.019667,
AUTHOR = {MASASHI KAWAMI, RYOKO YUMOTO, MIKIHISA TAKANO},
TITLE = {Preventive approach against drug-induced pulmonary fibrosis through the suppression of epithelial-mesenchymal transition},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {8},
PAGES = {1861--1865},
URL = {http://www.techscience.com/biocell/v46n8/47582},
ISSN = {1667-5746},
ABSTRACT = {A number of drugs induce pulmonary injury and subsequently lead to serious lung diseases such as pulmonary
fibrosis as the adverse drug reactions. However, an effective preventive approach against drug-induced pulmonary fibrosis
has not been established due to poor understanding of common preventive targets in a variety of drugs showing pulmonary
toxicity. Epithelial-mesenchymal transition (EMT), a cellular phenotypic change of the epithelial to mesenchymal state,
contributes to the development of pulmonary fibrosis through the conversion of damaged alveolar epithelium into
myofibroblasts. As several drugs with pulmonary toxicity have been reported to induce EMT, EMT serves as a bridge
between the drugs and pulmonary fibrosis. Accumulated evidence supports the potential of EMT as a preventive target
against drug-induced pulmonary fibrosis. Additionally, since there are mechanistic differences between the main
pharmacological effect and EMT induced by the drug, prevention based on EMT suppression would be possible and
would contribute to continuous clinical treatment with the drug to avoid EMT-mediated serious pulmonary fibrosis.
Furthermore, targeting EMT seems to be adequate for exerting a preventive effect since EMT in damaged alveolar
epithelial cells occurs prior to the development of the pathophysiological state of the whole lung in a bleomycin-induced
lung injury rat model. This viewpoint deals with the benefits and perspectives of preventive approaches against druginduced pulmonary fibrosis through the suppression of EMT, which has rarely been addressed.},
DOI = {10.32604/biocell.2022.019667}
}