GWAS in Fibrosing Interstitial Lung Disease
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ABSTRACT:
PROVIDER: PRJNA248931 | ENA |
REPOSITORIES: ENA
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Project description:The mechanisms and molecular pathways underlying interstitial lung diseases (ILDs) are poorly understood. Systems biology approaches were used to identify perturbed networks in these disease states to gain a better understanding of the underlying mechanisms of disease. Through profiling genes and miRNAs, we found subsets of genes and miRNAs that distinguish different disease stages, ILDs from controls, and idiopathic pulmonary fibrosis (IPF) from non-specific interstitial pneumonitis (NSIP). Traditional pathway analysis revealed several disease-associated modules involving genes from the TGF-beta, Wnt, focal adhesion and smooth muscle actin pathways that may be involved in advancing fibrosis. A comprehensively integrative approach was used to construct a global gene regulatory network based on the perturbation of key regulatory elements, transcriptional factors and miRNAs. The data also demonstrated that several subnetworks were significantly associated with key molecules involved in the diseases. We present a broad overview of the disease at a molecular level and discuss several possibly key regulatory molecular circuits that could play central roles in facilitating the progression of ILDs. Lung tissue samples from 23 patients with IPF or related disorders were obtained from the Lung Tissue Research Consortium (www.ltrcpublic.org). 11 samples came from patients who had been diagnosed with usual interstitial pneumonia/ idiopathic pulmonary fibrosis (UIP/IPF), 5 samples came from patients with non-specific interstitial pneumonia (NSIP), the remaining from patients with uncharacterized fibrosis and from patients with other ILD variants. B. Biopsies from uninvolved lung tissue from lung cancer patients (5 samples) and from one lung transplant patient were used as controls for comparison with the ILD samples.
2011-03-24 | E-GEOD-21369 | biostudies-arrayexpress
Project description:The mechanisms and molecular pathways underlying interstitial lung diseases (ILDs) are poorly understood. Systems biology approaches were used to identify perturbed networks in these disease states to gain a better understanding of the underlying mechanisms of disease. Through profiling genes and miRNAs, we found subsets of genes and miRNAs that distinguish different disease stages, ILDs from controls, and idiopathic pulmonary fibrosis (IPF) from non-specific interstitial pneumonitis (NSIP). Traditional pathway analysis revealed several disease-associated modules involving genes from the TGF-beta, Wnt, focal adhesion and smooth muscle actin pathways that may be involved in advancing fibrosis. A comprehensively integrative approach was used to construct a global gene regulatory network based on the perturbation of key regulatory elements, transcriptional factors and miRNAs. The data also demonstrated that several subnetworks were significantly associated with key molecules involved in the diseases. We present a broad overview of the disease at a molecular level and discuss several possibly key regulatory molecular circuits that could play central roles in facilitating the progression of ILDs. Lung tissue samples from thirty patients with IPF or related disorders were obtained from the Lung Tissue Research Consortium (www.ltrcpublic.org). Ten samples came from patients who had been diagnosed with usual interstitial pneumonia/ idiopathic pulmonary fibrosis (UIP/IPF), nine samples came from patients with non-specific interstitial pneumonia (NSIP), four from patients with uncharacterized fibrosis, and the remaining samples came from patients with other ILD variants. Biopsies from uninvolved lung tissue from lung cancer patients (5 samples) and from one lung transplant patient were used as controls for comparison with the ILD samples.
2011-04-19 | E-GEOD-21394 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE21369: Gene expression profiles of interstitial lung disease (ILD) patients GSE21394: MicroRNA expression profiles of interstitial lung disease (ILD) patients Refer to individual Series
2011-04-19 | E-GEOD-21411 | biostudies-arrayexpress
Project description:Fibrosing interstitial lung diseases (ILDs) encompass a diverse range of scarring disorders that lead to progressive lung failure. Previous gene expression profiling studies focused on idiopathic pulmonary fibrosis (IPF) and bulk tissue samples. We employed digital spatial profiling to gain new insights into the spatial resolution of gene expression across distinct lung microenvironments (LMEs) in IPF, chronic hypersensitivity pneumonitis (CHP) and non-specific interstitial pneumonia (NSIP). We identified differentially expressed genes between LMEs within each condition, and across histologically similar regions between conditions. Uninvolved areas in IPF and CHP were remarkably distinct from normal controls, and displayed potential therapeutic targets. Hallmarks LMEs of each condition retained a distinct gene signature, but these could not be reproduced in matched lung tissue samples. Based on these gene expression signatures and unsupervised clustering, we grouped previously unclassified ILD cases into NSIP or CHP. Lastly, we characterized a gene expression pattern associated with poor outcome . Overall, our work uniquely dissects gene expression profiles between LMEs within and across different types of fibrosing ILDs. This new spatial transcriptomics approach has the potential to reclassify unclassifiable cases, to qualify the transcriptional relevance of smaller biopsies for clinical use, and to predict outcome at the time of diagnosis.
2024-09-30 | GSE255174 | GEO
Project description:Evaluation of common profibrotic pathway across interstitial lung disease
| PRJNA967318 | ENA
Project description:Blood gene expression profiling of interstitial lung disease samples
| PRJNA1112334 | ENA
Project description:Fibrosing interstitial lung diseases (ILDs) encompass a diverse range of scarring disorders that lead to progressive lung failure. Previous gene expression profiling studies focused on idiopathic pulmonary fibrosis (IPF) and bulk tissue samples. We employed digital spatial profiling to gain new insights into the spatial resolution of gene expression across distinct lung microenvironments (LMEs) in IPF, chronic hypersensitivity pneumonitis (CHP) and non-specific interstitial pneumonia (NSIP). We identified differentially expressed genes between LMEs within each condition, and across histologically similar regions between conditions. Uninvolved areas in IPF and CHP were remarkably distinct from normal controls, and displayed potential therapeutic targets. Hallmarks LMEs of each condition retained a distinct gene signature, but these could not be reproduced in matched lung tissue samples. Based on these gene expression signatures and unsupervised clustering, we grouped previously unclassified ILD cases into NSIP or CHP. Lastly, we characterized a gene expression pattern associated with poor outcome . Overall, our work uniquely dissects gene expression profiles between LMEs within and across different types of fibrosing ILDs. This new spatial transcriptomics approach has the potential to reclassify unclassifiable cases, to qualify the transcriptional relevance of smaller biopsies for clinical use, and to predict outcome at the time of diagnosis.
2024-09-30 | GSE255173 | GEO
Project description:Fibrotic interstitial lung diseases (ILDs) are often challenging to diagnose and classify, but an accurate diagnosis has significant implications for both treatment and prognosis. A subset of patients with fibrotic ILD experience progressive deterioration in lung function, physical performance, and quality of life. Several risk factors for ILD progression have been reported, such as male sex, older age, lower baseline pulmonary function, and a radiological or pathological pattern of usual interstitial pneumonia. Morphological similarities, common underlying pathobiologic mechanisms, and the consistently progressive worsening of these patients support the concept of a progressive fibrosing (PF)-ILD phenotype that can be applied to a variety of ILD subtypes. The conventional approach has been to use antifibrotic medications in patients with idiopathic pulmonary fibrosis (IPF) and immunosuppressive medications in patients with other fibrotic ILD subtypes; however, recent clinical trials have suggested a favourable treatment response to antifibrotic therapy in a wider variety of fibrotic ILDs. This review summarizes the literature on the evaluation and management of patients with PF-ILD, and discusses questions relevant to applying recent clinicial trial findings to real-world practice.
| S-EPMC6988233 | biostudies-literature