Published online Jun 26, 2023. doi: 10.4330/wjc.v15.i6.293
Peer-review started: April 14, 2023
First decision: May 17, 2023
Revised: June 1, 2023
Accepted: June 13, 2023
Article in press: June 13, 2023
Published online: June 26, 2023
Processing time: 73 Days and 6 Hours
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with high mortality rate. Therefore, exploring potential therapeutic targets to meet the unmet needs of IPF patients is of great significance.
To explore potential targets for IPF treatment, as well as potential pathways and therapeutic methods.
Explore novel hub genes for IPF therapy. Whether TDO2 can be a therapeutic target for IPF.
We used public datasets (GSE53845, GSE47460, GSE24206, and GSE110147) to identify differentially expressed genes between IPF patients and healthy donors. Potential targets were considered based on multiple bioinformatics conditions, especially the correlation between hub genes and carbon monoxide diffusing capacity, forced vital capacity, and patient survival rate. The mRNA levels of the hub genes were determined through quantitative real-time polymerase chain reaction. Transforming growth factor-β (TGF-β) induced pulmonary fibrosis mouse model and the expression of TDO2 was observed before and after the addition of inhibitor.
This study identifies novel hub genes to explore for IPF treatment. TDO2 was upregulated in an experimental mouse model of TGF-β-induced pulmonary fibrosis and a TDO2 inhibitor effectively suppressed TGF-β-induced fibroblast activation.
TDO2 could be a potential target for treatment of IPF.
More complete work with animal models is needed, as the TDO2 gene is apparently upregulated by bleomycin treatment.