ArticleJCI insight2021
Dysregulated overexpression of Sox9 induces fibroblast activation in pulmonary fibrosis.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Emergence of fibrotic pericytes and their transcriptional regulation in pulmonary fibrosis.Nature communications · 2026Article
- High mobility group motif proteins' role in fibrosis, inflammation, and vascular injury in systemic sclerosis.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Single cell atlas decodes the molecular dynamics of scar repair after human rotator cuff tear.Bone research · 2026Article
- A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure.Nature cardiovascular research · 2026Article
- PLK1 inhibition by volasertib suppresses key transcriptional regulators underlying fibroblast activation and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- BMDx2: A Tool for Integrating Toxicogenomics-Based Dose-Dependency Analysis and AOP-Based Mechanistic Insights.Small methods · 2025Article
- Pattern of SOX9 expression in pleomorphic adenoma, carcinoma ex pleomorphic adenoma, and matrix-producing metaplastic carcinoma of the breast lends support to common biology.Virchows Archiv : an international journal of pathology · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.The Journal of clinical investigation · 2025Article
- Semaphorin 3E-Plexin D1 Axis Drives Lung Fibrosis through ErbB2-Mediated Fibroblast Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Promoting epithelial regeneration in chemically induced acute lung injury through Sox9-positive alveolar type 2 epithelial cells.Stem cell research & therapy · 2025Article
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- Single-cell RNA-seq uncovers lineage-specific regulatory alterations of fibroblasts and endothelial cells in ligamentum flavum hypertrophy.Frontiers in immunology · 2025Article
- Hidden liver-joint axis: HBV infection causes rheumatoid arthritis via TRAFD1 with imbalance of HBV X protein and trans-ferulic acid.Virulence · 2024Article
- Stable and oscillatory hypoxia differentially regulate invasibility of breast cancer associated fibroblasts.Mechanobiology in medicine · 2024Article
- HMGB1 derived from lung epithelial cells after cobalt nanoparticle exposure promotes the activation of lung fibroblasts.Nanotoxicology · 2024Article
- Profibrotic role of the SOX9-MMP10-ECM biosynthesis axis in the tracheal fibrosis after injury and repair.Genes & diseases · 2024Article
- The Modulation of Respiratory Epithelial Cell Differentiation by the Thickness of an Electrospun Poly-ε-Carprolactone Mesh Mimicking the Basement Membrane.International journal of molecular sciences · 2024Article
- Cell-type-specific and disease-associated expression quantitative trait loci in the human lung.Nature genetics · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal fibrotic lung disease associated with unremitting fibroblast activation including fibroblast-to-myofibroblast transformation (FMT), migration, resistance to apoptotic clearance, and excessive deposition of extracellular matrix (ECM) proteins in the distal lung parenchyma. Aberrant activation of lung-developmental pathways is associated with severe fibrotic lung disease; however, the mechanisms through which these pathways activate fibroblasts in IPF remain unclear. Sry-box transcription factor 9 (Sox9) is a member of the high-mobility group box family of DNA-binding transcription factors that are selectively expressed by epithelial cell progenitors to modulate branching morphogenesis during lung development. We demonstrate that Sox9 is upregulated via MAPK/PI3K-dependent signaling and by the transcription factor Wilms' tumor 1 in distal lung-resident fibroblasts in IPF. Mechanistically, using fibroblast activation assays, we demonstrate that Sox9 functions as a positive regulator of FMT, migration, survival, and ECM production. Importantly, our in vivo studies demonstrate that fibroblast-specific deletion of Sox9 is sufficient to attenuate collagen deposition and improve lung function during TGF-α-induced pulmonary fibrosis. Using a mouse model of bleomycin-induced pulmonary fibrosis, we show that myofibroblast-specific Sox9 overexpression augments fibroblast activation and pulmonary fibrosis. Thus, Sox9 functions as a profibrotic transcription factor in activating fibroblasts, illustrating the potential utility of targeting Sox9 in IPF treatment.
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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.