ArticleRespiratory research2018
Comprehensive gene expression profiling identifies distinct and overlapping transcriptional profiles in non-specific interstitial pneumonia and idiopathic pulmonary fibrosis.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03836417 (Molecular Diagnosis of Idiopathic Interstitial Pneumonias), which is not on this map. Cited by 72 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Molecular Diagnosis of Idiopathic Interstitial Pneumonias: a Prospective Study
Who cites it
72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- Transcriptomics of interstitial lung disease: a systematic review and meta-analysis.The European respiratory journal · 2025Pooled it
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- Cross talk between bacterial and human gene networks enriched using ncRNAs in IBD disease.Scientific reports · 2023Pooled it
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- Synergistic inhibition of the PI3K-AKT-mTOR signaling pathway in idiopathic pulmonary fibrosis by Sanleng-Ezhu: a multi-omics and experimental study.Functional & integrative genomics · 2026Article
- Integrated in vitro and multi-cohort cross-omics analysis of HTLV-1-associated lung pathology reveals a RelA-dependent mechanism for monocyte recruitment and differentiation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Deficiency of GCN5 exacerbates pulmonary fibrosis by disrupting the LKB1-AMPK pathway.Cell communication and signaling : CCS · 2026Article
- Mitophagy promotes lung repair and regeneration by restoring epithelial metabolic fitness.Nature communications · 2026Article
- Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2.International journal of molecular medicine · 2026Article
- MUUMI: an R package for statistical and network-based meta-analysis for multi-omics data integration.BMC bioinformatics · 2026Article
- Advances in diagnosis of lung fibrosis: focus on present and future approaches.Frontiers in medicine · 2026Review
- Curated and harmonised transcriptomics datasets of interstitial lung diseases.Data in brief · 2025Article
- Article
- GPR40 activation alleviates pulmonary fibrosis by repressing M2 macrophage polarization through the PKD1/CD36/TGF-β1 pathway.Acta pharmacologica Sinica · 2025Article
- LMO7 drives profibrotic fibroblast polarization and pulmonary fibrosis in mice through TGF-β signalling.Acta pharmacologica Sinica · 2025Article
- Prediction model of mitochondrial energy metabolism related genes in idiopathic pulmonary fibrosis and its correlation with immune microenvironment.Scientific reports · 2025Article
- Identification of Ferroptosis-Inflammation Related Hub Genes and the Disease Subtypes in Idiopathic Pulmonary Fibrosis via System Biology Approaches.Molecular biotechnology · 2025Article
- Advances in idiopathic pulmonary fibrosis diagnosis and treatment.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Article
- PLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.Communications biology · 2025Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe clinical-radiographic distinction between idiopathic pulmonary fibrosis (IPF) and non-specific interstitial pneumonia (NSIP) is challenging. We sought to investigate the gene expression profiles of IPF and NSIP vs. normal controls.
methodsGene expression from explanted lungs of patients with IPF (n = 22), NSIP (n = 10) and from normal controls (n = 11) was assessed. Microarray analysis included Significance Analysis of Microarray (SAM), Ingenuity Pathway, Gene-Set Enrichment and unsupervised hierarchical clustering analyses. Immunohistochemistry and serology of proteins of interest were conducted.
resultsNSIP cases were significantly enriched for genes related to mechanisms of immune reaction, such as T-cell response and recruitment of leukocytes into the lung compartment. In IPF, in contrast, these involved senescence, epithelial-to-mesenchymal transition, myofibroblast differentiation and collagen deposition. Unlike the IPF group, NSIP cases exhibited a strikingly homogenous gene signature. Clustering analysis identified a subgroup of IPF patients with intermediate and ambiguous expression of SAM-selected genes, with the interesting upregulation of both NSIP-specific and senescence-related genes. Immunohistochemistry for p16, a senescence marker, on fibroblasts differentiated most IPF cases from NSIP. Serial serum levels of periostin, a senescence effector, predicted clinical progression in a cohort of patients with IPF.
conclusionsComprehensive gene expression profiling in explanted lungs identifies distinct transcriptional profiles and differentially expressed genes in IPF and NSIP, supporting the notion of NSIP as a standalone condition. Potential gene and protein markers to discriminate IPF from NSIP were identified, with a prominent role of senescence in IPF. The finding of a subgroup of IPF patients with transcriptional features of both NSIP and senescence raises the hypothesis that "senescent" NSIP may represent a risk factor to develop superimposed IPF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.