ArticleBMC medical genetics2017
Gene expression profiling of idiopathic interstitial pneumonias (IIPs): identification of potential diagnostic markers and therapeutic targets.
Article in BMC medical genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Transcriptomics of interstitial lung disease: a systematic review and meta-analysis.The European respiratory journal · 2025Pooled it
- Pooled it
- Research on the role and mechanism of SLC7A5 in idiopathic pulmonary fibrosis.Molecular medicine reports · 2026Article
- Mucus plugs-associated gene expression identifies pathophysiology shared with chronic bronchitis.American journal of respiratory and critical care medicine · 2026Article
- Systemic miR-26a deficiency attenuates pulmonary fibrosis via PTEN upregulation and downstream TIMP-1 suppression.Molecular therapy. Nucleic acids · 2025Article
- Molecular Hydrogen Ameliorates Anti-Desmoglein 1 Antibody-Induced Pemphigus-Associated Interstitial Lung Disease by Inhibiting Oxidative Stress.International journal of molecular sciences · 2025Article
- Genome-wide CRISPR/Cas9 screening identifies key profibrotic regulators of TGF-β1-induced epithelial-mesenchymal transformation and pulmonary fibrosis.Frontiers in molecular biosciences · 2025Article
- Mucus and mucin: changes in the mucus barrier in disease states.Tissue barriers · 2025Review
- The Role of Ubiquitin-Proteasome System (UPS) in Asthma Pathology.Journal of asthma and allergy · 2025Review
- Hypoxia-inducible factor 1α modulates interstitial pneumonia-mediated lung cancer progression.Journal of translational medicine · 2023Article
- The Interaction of OTUB1 and TRAF3 Mediates NLRP3 Inflammasome Activity to Regulate TGF-β1-induced BEAS-2B Cell Injury.Applied biochemistry and biotechnology · 2023Article
- Fibroblast Upregulation of Vitamin D Receptor Represents a Self-Protective Response to Limit Fibroblast Proliferation and Activation during Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2023Article
- Alveolar epithelial cells are competent producers of interstitial extracellular matrix with disease relevant plasticity in a human in vitro 3D model.Scientific reports · 2023Article
- Identification of hub genes associated with COVID-19 and idiopathic pulmonary fibrosis by integrated bioinformatics analysis.PloS one · 2022Article
- Article
- miR-21 Exerts Anti-proliferative and Pro-apoptotic Effects in LPS-induced WI-38 Cells via Directly Targeting TIMP3.Cell biochemistry and biophysics · 2021Article
- Pathogenetic profiling of COVID-19 and SARS-like viruses.Briefings in bioinformatics · 2021Article
- Gene Targets Network Analysis for the Revealing and Guidance of Molecular Driving Mechanism of Lung Cancer.Frontiers in genetics · 2021Article
- IL-18 binding protein can be a prognostic biomarker for idiopathic pulmonary fibrosis.PloS one · 2021Article
- Dual Effect of Bleomycin on Histopathological Features of Lungs and Mediastinal Fat-Associated Lymphoid Clusters in an Autoimmune Disease Mouse Model.Frontiers in immunology · 2021Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic fibrosing idiopathic interstitial pneumonia (IIP) is characterized by alveolar epithelial damage, activation of fibroblast proliferation, and loss of normal pulmonary architecture and function. This study aims to investigate the genetic backgrounds of IIP through gene expression profiling and pathway analysis, and to identify potential biomarkers that can aid in diagnosis and serve as novel therapeutic targets.
methodsRNA extracted from lung specimens of 12 patients with chronic fibrosing IIP was profiled using Illumina Human WG-6 v3 BeadChips, and Ingenuity Pathway Analysis was performed to identify altered functional and canonical signaling pathways. For validating the results from gene expression analysis, immunohistochemical staining of 10 patients with chronic fibrosing IIP was performed.
resultsNinety-eight genes were upregulated in IIP patients relative to control subjects. Some of the upregulated genes, namely desmoglein 3 (DSG3), protocadherin gamma-A9 (PCDHGA9) and discoidin domain-containing receptor 1 (DDR1) are implicated in cell-cell interaction and/or adhesion; some, namely collagen type VII, alpha 1 (COL7A1), contactin-associated protein-like 3B (CNTNAP3B) and mucin-1 (MUC1) are encoding the extracellular matrix molecule or the molecules involved in cell-matrix interactions; and the others, namely CDC25C and growth factor independent protein 1B (GFI1B) are known to affect cell proliferation by affecting the progression of cell cycle or regulating transcription. According to pathway analysis, alternated pathways in IIP were related to cell death and survival and cellular growth and proliferation, which are more similar to cancer than to inflammatory response and immunological diseases. Using immunohistochemistry, we further validate that DSG3, the most highly upregulated gene, shows higher expression in chronic fibrosing IIP lung as compared to control lung.
conclusionWe identified several genes upregulated in chronic fibrosing IIP patients as compared to control, and found genes and pathways implicated in cancer, rather than in inflammatory or immunological disease to play important roles in the pathogenesis of IIPs. Moreover, DSG3 is a novel potential biomarker for chronic fibrosing IIP with its significantly high expression in IIP lung.
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