ArticlePloS one2021
Lung gene expression and single cell analyses reveal two subsets of idiopathic pulmonary fibrosis (IPF) patients associated with different pathogenic mechanisms.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- DPEP1 promotes pulmonary fibrosis by regulating arachidonic acid metabolism.Journal of thoracic disease · 2026Article
- Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026Review
- Next-Generation Sequencing in Pulmonary Fibrosis: Translational Promise and Current Clinical Limitations.Current issues in molecular biology · 2026Review
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Survival impact and safety comparison of pirfenidone and nintedanib for idiopathic pulmonary fibrosis: A meta-analysis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025Article
- Adoptive Transfer of T Cells as a Potential Therapeutic Approach in the Bleomycin-Injured Mouse Lung.The journal of gene medicine · 2025Article
- Common biomarkers of idiopathic pulmonary fibrosis and systemic sclerosis based on WGCNA and machine learning.Scientific reports · 2025Article
- An Overview of the Role of Genetic factors in Idiopathic Pulmonary Fibrosis: Insights from Epidemiology to Prognosis.International journal of medical sciences · 2025Review
- Review
- Article
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- Single-cell reference mapping to construct and extend cell-type hierarchies.NAR genomics and bioinformatics · 2023Article
- Standard of care drugs do not modulate activity of senescent primary human lung fibroblasts.Scientific reports · 2023Article
- PEDF is an antifibrosis factor that inhibits the activation of fibroblasts in a bleomycin-induced pulmonary fibrosis rat model.Respiratory research · 2022Article
- Immunophenotyping of Acute Inflammatory Exacerbations of Lung Injury Driven by Mutant Surfactant Protein-C: A Role for Inflammatory Eosinophils.Frontiers in pharmacology · 2022Article
- Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Integrative analysis of lung molecular signatures reveals key drivers of idiopathic pulmonary fibrosis.BMC pulmonary medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis is a progressive and debilitating lung disease with large unmet medical need and few treatment options. We describe an analysis connecting single cell gene expression with bulk gene expression-based subsetting of patient cohorts to identify IPF patient subsets with different underlying pathogenesis and cellular changes. We reproduced earlier findings indicating the existence of two major subsets in IPF and showed that these subsets display different alterations in cellular composition of the lung. We developed classifiers based on the cellular changes in disease to distinguish subsets. Specifically, we showed that one subset of IPF patients had significant increases in gene signature scores for myeloid cells versus a second subset that had significantly increased gene signature scores for ciliated epithelial cells, suggesting a differential pathogenesis among IPF subsets. Ligand-receptor analyses suggested there was a monocyte-macrophage chemoattractant axis (including potentially CCL2-CCR2 and CCL17-CCR4) among the myeloid-enriched IPF subset and a ciliated epithelium-derived chemokine axis (e.g. CCL15) among the ciliated epithelium-enriched IPF subset. We also found that these IPF subsets had differential expression of pirfenidone-responsive genes suggesting that our findings may provide an approach to identify patients with differential responses to pirfenidone and other drugs. We believe this work is an important step towards targeted therapies and biomarkers of response.
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