ArticleScientific reports2022
PD-L1 mediates lung fibroblast to myofibroblast transition through Smad3 and β-catenin signaling pathways.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Prognostic impact of interstitial lung abnormalities in lung cancer: a systematic review and meta-analysis.Frontiers in oncology · 2024Pooled it
- Bispecific targeting of CHI3L1 and PD-1 as a therapeutic strategy for pulmonary fibrosis.JCI insight · 2026Article
- Dual Modulation of Senescence and Immune Checkpoints by Metformin and Dapagliflozin Attenuates Liver Fibrosis in a Thioacetamide-Induced Rat Model.Advanced pharmaceutical bulletin · 2026Article
- Advances in infection-immunity mechanisms and molecular regulatory networks in severe pneumonia-associated lung injury.Frontiers in immunology · 2026Review
- Development of peribronchiolar fibrosis is associated with local immune and MAPK pathway activation in a murine model of deployment-related constrictive bronchiolitis.Frontiers in public health · 2026Article
- Integration of single-cell and bulk transcriptomics uncovers CHST6 as a shared pathogenic driver in idiopathic pulmonary fibrosis and lung cancer.APL bioengineering · 2025Article
- BRD4 Mediates Transforming Growth Factor-β-Induced Smooth Muscle Cell Differentiation from Mesenchymal Progenitor Cells.International journal of molecular sciences · 2025Article
- The Activity of Human NK Cells Towards 3D Heterotypic Cellular Tumor Model of Breast Cancer.Cells · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- Facilitation of diabetic wound healing by far upstream element binding protein 1 through augmentation of dermal fibroblast activity.Acta diabetologica · 2025Article
- Article
- Recent progress in exosomal non-coding RNAs research related to idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Review
- Outcome of immune checkpoint inhibitor treatment in non-small cell lung cancer patients with interstitial lung abnormalities: clinical utility of subcategorizing interstitial lung abnormalities.Cancer immunology, immunotherapy : CII · 2024Article
- Pathological examination of factors involved in PD-L1 expression in patients with oral tongue squamous cell carcinoma.Maxillofacial plastic and reconstructive surgery · 2024Article
- Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024Review
- Persistence of lung structural and functional alterations at one year post-COVID-19 is associated with increased serum PD-L2 levels and altered CD4/CD8 ratio.Immunity, inflammation and disease · 2024Article
- The role of the immunosuppressive PD-1/PD-L1 checkpoint pathway in the aging process and age-related diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Anti-PD-L1 Immunotherapy of Chronic Virus Infection Improves Virus Control without Augmenting Tissue Damage by Fibrosis.Viruses · 2024Article
- HE4-based nomogram for predicting overall survival in patients with idiopathic pulmonary fibrosis: construction and validation.European journal of medical research · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Programmed death ligand-1 (PD-L1) is an immune checkpoint protein that has been linked with idiopathic pulmonary fibrosis (IPF) and fibroblast to myofibroblast transition (FMT). However, it remains largely unclear how PD-L1 mediates this process. We found significantly increased PD-L1 in the lungs of idiopathic pulmonary fibrosis patients and mice with pulmonary fibrosis induced by bleomycin and TGF-β. In primary human lung fibroblasts (HLFs), TGF-β induced PD-L1 expression that is dependent on both Smad3 and p38 pathways. PD-L1 knockdown using siRNA significantly attenuated TGF-β-induced expression of myofibroblast markers α-SMA, collagen-1, and fibronectin in normal and IPF HLFs. Further, we found that PD-L1 interacts with Smad3, and TGF-β induces their interaction. Interestingly, PD-L1 knockdown reduced α-SMA reporter activity induced by TGF-β in HLFs, suggesting that PD-L1 might act as a co-factor of Smad3 to promote target gene expression. TGF-β treatment also phosphorylates GSK3β and upregulates β-catenin protein levels. Inhibiting β-catenin signaling with the pharmaceutical inhibitor ICG001 significantly attenuated TGF-β-induced FMT. PD-L1 knockdown also attenuated TGF-β-induced GSK3β phosphorylation/inhibition and β-catenin upregulation, implicating GSK3β/β-catenin signaling in PD-L1-mediated FMT. Collectively, our findings demonstrate that fibroblast PD-L1 may promote pulmonary fibrosis through both Smad3 and β-catenin signaling and may represent a novel interventional target for IPF.
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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.