ArticleLaboratory investigation; a journal of technical methods and pathology2020
The Shh/Gli signaling cascade regulates myofibroblastic activation of lung-resident mesenchymal stem cells via the modulation of Wnt10a expression during pulmonary fibrogenesis.
Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- A Multispecies, Modality-Agnostic Scalable In Vivo Mosaic Screening Platform for Therapeutic Target Discovery.bioRxiv : the preprint server for biology · 2026Article
- Muscle transcriptome profiling reveals novel molecular pathways and biomarkers in laminin-α2 deficient patients.Acta neuropathologica communications · 2026Article
- Study of the Immune Infiltration and Sonic Hedgehog Expression Mechanism in Synovial Tissue of Rheumatoid Arthritis-Related Interstitial Lung Disease under Machine Learning CIBERSORT Algorithm.Molecular biotechnology · 2025Article
- Emerging Concepts in Fibroblast Biology and Progressive Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- The influence of asthmatic inflammation and house dust mite (HDM) exposure on abundance, immune-modulatory potential, and differentiation capacity of the lung-resident mesenchymal stem cells (lrMSCs).Stem cell research & therapy · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- CT-sensitized nanoprobe for effective early diagnosis and treatment of pulmonary fibrosis.Journal of nanobiotechnology · 2025Article
- Tissue Mechanics and Hedgehog Signaling Crosstalk as a Key Epithelial-Stromal Interplay in Cancer Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Stem cell-based therapy for fibrotic diseases: mechanisms and pathways.Stem cell research & therapy · 2024Review
- Current state of signaling pathways associated with the pathogenesis of idiopathic pulmonary fibrosis.Respiratory research · 2024Review
- Circadian regulation of cancer stem cells and the tumor microenvironment during metastasis.Nature cancer · 2024Review
- NLRP3 inflammasome mediates abnormal epithelial regeneration and distal lung remodeling in silica‑induced lung fibrosis.International journal of molecular medicine · 2024Article
- Targeting Progression in Pulmonary Fibrosis: An Overview of Underlying Mechanisms, Molecular Biomarkers, and Therapeutic Intervention.Life (Basel, Switzerland) · 2024Review
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- Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- The Role of Lung Resident Mesenchymal Stromal Cells in the Pathogenesis and Repair of Chronic Lung Disease.Stem cells (Dayton, Ohio) · 2023Review
- Perinatal origins of bronchopulmonary dysplasia-deciphering normal and impaired lung development cell by cell.Molecular and cellular pediatrics · 2023Review
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung-resident mesenchymal stem cells (LR-MSCs) are important regulators of lung repair and regeneration, and evidence suggests that this cell population also plays a vital role in fibrosis. Crosstalk between sonic hedgehog (Shh) signaling and wingless/integrated (Wnt) has been demonstrated in idiopathic pulmonary fibrosis (IPF). However, the underlying correlation between LR-MSCs and the Shh-Wnt signaling cascade remains poorly understood. Here, we identified Wnt10a as a key factor in pulmonary fibrosis. Using a bleomycin mouse model, we found that highly expressed Wnt10a was secreted by LR-MSCs undergoing myofibroblastic differentiation. LR-MSCs with myofibroblast characteristics isolated from fibrotic lungs exhibited increased Shh pathway activity, suggesting their role as Shh targets. In vitro, LR-MSCs responded to stimulation by recombinant Shh, acquiring a myofibroblast phenotype. We further demonstrated that the Shh/glioblastoma (Gli) system machinery regulated LR-MSC-to-myofibroblast transition and pulmonary fibrosis via manipulation of Wnt/β-catenin signaling. Accordingly, inhibition of the Shh-Wnt signaling cascade prevented LR-MSC transformation into myofibroblasts and ameliorated pulmonary fibrotic lesions. Moreover, induction of Wnt10a expression and activation of Shh/Gli signaling were confirmed in human pulmonary fibrosis. In summary, this study linking the Shh-Wnt signaling cascade with LR-MSC fibrogenic activity furthered the current understanding of pulmonary fibrosis pathogenesis and might provide a new perspective in the development of treatment strategies for IPF.
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