Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive disease whose etiology remains unknown. The purpose of this study was to explore hub genes and pathways related to IPF development and prognosis. Multiple gene expression datasets were downloaded from the Gene Expression Omnibus database. Weighted correlation network analysis (WGCNA) was performed and differentially expressed genes (DEGs) identified to investigate Hub modules and genes correlated with IPF. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and protein-protein interaction (PPI) network analysis were performed on selected key genes. In the PPI network and cytoHubba plugin, 11 hub genes were identified, including ASPN, CDH2, COL1A1, COL1A2, COL3A1, COL14A1, CTSK, MMP1, MMP7, POSTN, and SPP1. Correlation between hub genes was displayed and validated. Expression levels of hub genes were verified using quantitative real-time PCR (qRT-PCR). Dysregulated expression of these genes and their crosstalk might impact the development of IPF through modulating IPF-related biological processes and signaling pathways. Among these genes, expression levels of COL1A1, COL3A1, CTSK, MMP1, MMP7, POSTN, and SPP1 were positively correlated with IPF prognosis. The present study provides further insights into individualized treatment and prognosis for IPF.
Highlights
Idiopathic pulmonary fibrosis (IPF), a chronic and progressive lung disease of unknown etiology (King et al, 2014; Martinez et al, 2017; Raghu et al, 2018), is characterized by diffuse alveolar inflammation and alveolar structural damage (Xu et al, 2016; Claude and Harold, 2018; David et al, 2019)
Before the removal of batch effects, samples were clustered by batches based on the first two principal components (PC) of unnormalized expression values (Figures 1A,C)
The scatter plot of principal component analysis (PCA) based on normalized expression showed that batch processing effects from different platforms were eliminated (Figures 1B,D)
Summary
Idiopathic pulmonary fibrosis (IPF), a chronic and progressive lung disease of unknown etiology (King et al, 2014; Martinez et al, 2017; Raghu et al, 2018), is characterized by diffuse alveolar inflammation and alveolar structural damage (Xu et al, 2016; Claude and Harold, 2018; David et al, 2019). The global annual incidence of IPF is 0.2–93.7 per 100,000 (Hutchinson et al, 2015) and the median survival time is only 2–3 years after diagnosis is confirmed (Tran and Suissa, 2018; Schäfer et al, 2020). Clinical biomarkers reliably reflecting the progression of IPF are small in number.
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