ArticleRespiratory research2015
Down-regulation of USP13 mediates phenotype transformation of fibroblasts in idiopathic pulmonary fibrosis.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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The trial behind it
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Transcriptomics of interstitial lung disease: a systematic review and meta-analysis.The European respiratory journal · 2025Pooled it
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- MUUMI: an R package for statistical and network-based meta-analysis for multi-omics data integration.BMC bioinformatics · 2026Article
- Integrated metabolomic and transcriptomic profiling reveals lipid dysregulation and potential biomarkers in interstitial lung disease.Frontiers in immunology · 2026Article
- Curated and harmonised transcriptomics datasets of interstitial lung diseases.Data in brief · 2025Article
- Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review).Oncology letters · 2024Review
- Fibroblast Upregulation of Vitamin D Receptor Represents a Self-Protective Response to Limit Fibroblast Proliferation and Activation during Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2023Article
- USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Autophagy in Idiopathic Pulmonary Fibrosis: Predisposition of the Aging Lung to Fibrosis?American journal of respiratory cell and molecular biology · 2023Article
- CK2-Mediated Phosphorylation Upregulates the Stability of USP13 and Promotes Ovarian Cancer Cell Proliferation.Cancers · 2022Article
- PKM2 promotes pulmonary fibrosis by stabilizing TGF-β1 receptor I and enhancing TGF-β1 signaling.Science advances · 2022Article
- miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- PTEN: An Emerging Potential Target for Therapeutic Intervention in Respiratory Diseases.Oxidative medicine and cellular longevity · 2022Review
- Role of USP13 in physiology and diseases.Frontiers in molecular biosciences · 2022Review
- Transcriptomic-Based Quantification of the Epithelial-Hybrid-Mesenchymal Spectrum across Biological Contexts.Biomolecules · 2021Article
- MUC16 Is Overexpressed in Idiopathic Pulmonary Fibrosis and Induces Fibrotic Responses Mediated by Transforming Growth Factor-β1 Canonical Pathway.International journal of molecular sciences · 2021Article
- Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.Journal of the American Society of Nephrology : JASN · 2021Article
- Ferroptosis-Related Genes in Bronchoalveolar Lavage Fluid Serves as Prognostic Biomarkers for Idiopathic Pulmonary Fibrosis.Frontiers in medicine · 2021Article
- Deubiquitinase USP13 promotes extracellular matrix expression by stabilizing Smad4 in lung fibroblast cells.Translational research : the journal of laboratory and clinical medicine · 2020Article
- The Role of Deubiquitinating Enzymes in Acute Lung Injury and Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by fibroblastic foci and progressive scarring of the pulmonary parenchyma. IPF fibroblasts display increased proliferation and enhanced migration and invasion, analogous to cancer cells. This transformation-like phenotype of fibroblasts plays an important role in the development of pulmonary fibrosis, but the mechanism for this is not well understood.
methodsIn this study, we compared gene expression profiles in fibrotic lung tissues from IPF patients and normal lung tissues from patients with primary spontaneous pneumothorax using a cDNA microarray to examine the mechanisms involved in the pathogenesis of IPF. In a cDNA microarray, we found that USP13 was decreased in lung tissues from patients with IPF, which was further confirmed by results from immunohistochemistry and western blot assays. Then, we used RNA interference in MRC-5 cells to inhibit USP13 and evaluated its effects by western blot, real-time RT-PCR, bromodeoxyuridine incorporation, and transwell assays. We also used co-immunoprecipitation and immunofluorescence staining to identify the correlation between USP13 and PTEN in IPF.
resultsUSP13 expression levels were markedly reduced in fibroblastic foci and primary IPF fibroblast lines. The depletion of USP13 resulted in the transformation of fibroblasts into an aggressive phenotype with enhanced proliferative, migratory, and invasive capacities. Additionally, USP13 interacted with PTEN and mediated PTEN ubiquitination and degradation in lung fibroblasts.
conclusionsDown-regulation of USP13 mediates PTEN protein loss and fibroblast phenotypic change, and thereby plays a crucial role in IPF pathogenesis.
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