ArticlePLoS medicine2005
Up-regulation and profibrotic role of osteopontin in human idiopathic pulmonary fibrosis.
Article in PLoS medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 288 papers, 4 of them syntheses that pooled it.
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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
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Who cites it
288 citing papers in PubMed, 4 syntheses or guidelines pooled it, 498 citations in OpenAlex.
- Transcriptomics of interstitial lung disease: a systematic review and meta-analysis.The European respiratory journal · 2025Pooled it
- Shared and unique transcriptomic signature genes and pathways among biopsy, peripheral blood mononuclear cells and bronchoalveolar lavage samples in IPF patients revealed using comparative meta-transcriptome analysis.Tuberkuloz ve toraks · 2024Pooled it
- Gene expression meta-analysis reveals aging and cellular senescence signatures in scleroderma-associated interstitial lung disease.Frontiers in immunology · 2024Pooled it
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- Osteopontin Links Myeloid Activation and Disease Progression in Systemic Sclerosis.Cell reports. Medicine · 2020Trial
- Airway microbiota signals anabolic and catabolic remodeling in the transplanted lung.The Journal of allergy and clinical immunology · 2018Trial
- Collaborative functionality between three types of inflammation in idiopathic pulmonary fibrosis.Nature immunology · 2026Review
- Pulmonary responses to polyacrylic acid with and without carboxyl groups following intratracheal instillation in rats.Archives of toxicology · 2026Article
- Article
- Next-Generation Sequencing in Pulmonary Fibrosis: Translational Promise and Current Clinical Limitations.Current issues in molecular biology · 2026Review
- Single-cell RNA sequencing reveals aberrant airway epithelial-immune cell cross-talk in pulmonary fibrosis.ERJ open research · 2026Article
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Alveolar-Basal Intermediates Drive Pulmonary Fibrosis via Coordination of a Pro-Fibrotic Signaling Niche in Silicosis.bioRxiv : the preprint server for biology · 2026Article
- Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- An hiPSC-derived multi-lineage lung model exhibiting proximal-distal epithelial features for modeling pulmonary fibrosis.Frontiers in cell and developmental biology · 2026Article
- Role of Scar-Associated Macrophages in Organ Fibrosis Diseases.Journal of immunology research · 2026Review
- Single-cell resolution spatial analysis of antigen-presenting cancer-associated fibroblast niches.Cancer cell · 2025Article
- A serum biomarker-based index for predicting progressive pulmonary fibrosis in patients with anti-synthetase syndrome: the LOCCM index.Respiratory research · 2025Article
228 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive and lethal disorder characterized by fibroproliferation and excessive accumulation of extracellular matrix in the lung. METHODS AND
findingsUsing oligonucleotide arrays, we identified osteopontin as one of the genes that significantly distinguishes IPF from normal lungs. Osteopontin was localized to alveolar epithelial cells in IPF lungs and was also significantly elevated in bronchoalveolar lavage from IPF patients. To study the fibrosis-relevant effects of osteopontin we stimulated primary human lung fibroblasts and alveolar epithelial cells (A549) with recombinant osteopontin. Osteopontin induced a significant increase of migration and proliferation in both fibroblasts and epithelial cells. Epithelial growth was inhibited by the pentapeptide Gly-Arg-Gly-Asp-Ser (GRGDS) and antibody to CD44, while fibroproliferation was inhibited by GRGDS and antibody to alphavbeta3 integrin. Fibroblast and epithelial cell migration were inhibited by GRGDS, anti-CD44, and anti-alphavbeta3. In fibroblasts, osteopontin up-regulated tissue inhibitor of metalloprotease-1 and type I collagen, and down-regulated matrix metalloprotease-1 (MMP-1) expression, while in A549 cells it caused up-regulation of MMP-7. In human IPF lungs, osteopontin colocalized with MMP-7 in alveolar epithelial cells, and application of weakest link statistical models to microarray data suggested a significant interaction between osteopontin and MMP-7.
conclusionsOur results provide a potential mechanism by which osteopontin secreted from the alveolar epithelium may exert a profibrotic effect in IPF lungs and highlight osteopontin as a potential target for therapeutic intervention in this incurable disease.
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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.