Abstract
Idiopathic pulmonary fibrosis (IPF) is a lethal, agnogenic interstitial lung disease with limited therapeutic options. To investigate vital genes involved in the development of IPF, we integrated and compared four expression profiles (GSE110147, GSE53845, GSE24206, and GSE10667), including 87 IPF samples and 40 normal samples. By reanalyzing these datasets, we managed to identify 62 upregulated genes and 20 downregulated genes in IPF samples compared with normal samples. Differentially expressed genes (DEGs) were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to illustrate relevant pathways of IPF, biological processes, molecular function, and cell components. The DEGs were then subjected to protein–protein interaction (PPI) for network analysis, serving to find 11 key candidate genes (ANXA3, STX11, THBS2, MMP1, MMP9, MMP7, MMP10, SPP1, COL1A1, ITGB8, IGF1). The result of RT-qPCR and immunohistochemical staining verified our finding as well. In summary, we identified 11 key candidate genes related to the process of IPF, which may contribute to novel treatments of IPF.
Highlights
11 key candidate genes related to the process of Idiopathic pulmonary fibrosis (IPF), which may contribute to novel treatments of IPF
The analysis showed that there are 11 core genes participating in the pathological changes of IPF, in which ANXA3 and STX11 are downregulated genes while THBS2, MMP1, MMP9, MMP7, MMP10, SPP1, COL1A1, ITGB8, and IGF1 are upregulated genes
The mechanisms underlying the pathogenesis of IPF are quite complex and remain incompletely understood
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Idiopathic pulmonary fibrosis (IPF) is a chronic, devastating, progressive, and fibrotic interstitial lung disease of unknown etiology with few treatment options. IPF occurs primarily in middle-aged and elderly adults, and its median survival time varies from three to five years after diagnosis [1]. The main clinical features of IPF are inexorable decline in lung function, progressive respiratory failure, and high mortality. A nonproductive cough and progressive exertional dyspnea are key symptoms of IPF. The important physical findings are scalene muscle hypertrophy, bibasilar fine crackles, and finger clubbing
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