Wang R, Yang YM. Identification of potential biomarkers for idiopathic pulmonary fibrosis and validation of TDO2 as a potential therapeutic target. World J Cardiol 2023; 15(6): 293-308 [PMID: 37397828 DOI: 10.4330/wjc.v15.i6.293]
Corresponding Author of This Article
Yan-Mei Yang, PhD, Doctor, Zhengzhou University, Research Centre of Basic Medicine, Academy of Medical Sciences, No. 40 North University Road, Erqi District, Zhengzhou 450000, Henan Province, China. yang_yanmei@gs.zzu.edu.cn
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. Jun 26, 2023; 15(6): 293-308 Published online Jun 26, 2023. doi: 10.4330/wjc.v15.i6.293
Identification of potential biomarkers for idiopathic pulmonary fibrosis and validation of TDO2 as a potential therapeutic target
Ru Wang, Yan-Mei Yang
Ru Wang, Henan University of Chinese Medicine, Collaborative Innovation Centre for Chinese Medicine and Respiratory Diseases, Zhengzhou 450046, Henan Province, China
Yan-Mei Yang, Zhengzhou University, Research Centre of Basic Medicine, Academy of Medical Sciences, Zhengzhou 450000, Henan Province, China
Author contributions: Yang YM designed the research study; Wang R and Yang YM performed the research; Yang YM analysed the data and wrote the manuscript; Wang R performed the experiment research; all authors have read and approved the final manuscript.
Institutional review board statement: Our manuscript involves experiments on mice, as well as the A549 and IMR-90 cell lines, but does not involve any human experimentation.
Institutional animal care and use committee statement: The study was reviewed and approved by the Experimental Animal Ethics Committee of Henan University of Chinese Medicine, No. DWLLGZR202202036.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The authors confirm that the data supporting the findings of this study are available.
ARRIVE guidelines statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Yan-Mei Yang, PhD, Doctor, Zhengzhou University, Research Centre of Basic Medicine, Academy of Medical Sciences, No. 40 North University Road, Erqi District, Zhengzhou 450000, Henan Province, China. yang_yanmei@gs.zzu.edu.cn
Received: April 14, 2023 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
ARTICLE HIGHLIGHTS
Research background
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.
Research motivation
To explore potential targets for IPF treatment, as well as potential pathways and therapeutic methods.
Research objectives
Explore novel hub genes for IPF therapy. Whether TDO2 can be a therapeutic target for IPF.
Research methods
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.
Research results
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.
Research conclusions
TDO2 could be a potential target for treatment of IPF.
Research perspectives
More complete work with animal models is needed, as the TDO2 gene is apparently upregulated by bleomycin treatment.
