ArticleNature communications2025
Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models.
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Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23citing papers in PubMed
–field-weighted citation impact
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Who cites it
23 citing papers in PubMed.
- Nanozyme-crosslinked dual-network hydrogel enables multi-stage modulation of the dysregulated repair cascade for regenerative wound healing.Bioactive materials · 2026Article
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- Hardened ground: ECM stiffness as a unifying biomechanical driver of reproductive stem cell aging.Biogerontology · 2026Review
- Cytoskeletal-nuclear control of alveolar fibroblast identity directs lung regeneration.bioRxiv : the preprint server for biology · 2026Article
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Effects of LATS1/2 kinases inhibition on lung epithelial cells in a regeneration model.Molecular and cellular biochemistry · 2026Article
- Unleashing innovative cross-organ fibrosis therapies by harnessing the omics revolution.JCI insight · 2026Review
- Shared mechanisms of organ fibrosis.JCI insight · 2026Review
- Integrative single-cell and bulk transcriptomic analyses identifyJournal of thoracic disease · 2026Article
- Expression of Lysyl Oxidase-Related Protein and Effect of Lysyl Oxidase Inhibition in Cyclosporine-Induced Nephropathy Mouse Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- 2025 annual review of basic and translational research advances in pulmonary fibrosis: a narrative review.Journal of thoracic disease · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Expanding the toolbox to develop IAP-based degraders of TEAD transcription factors.Communications chemistry · 2026Article
- Review
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis.Theranostics · 2026Article
- Review
- Angiotensin II Activates Yes-Associated Protein (YAP) in Fibroblast Promoting Deep Fascia Remodeling.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
34 authors.
Darcy Elizabeth WagnerLund Stem Cell Center, Faculty of Medicine, Lund University, Lund, Sweden. darcy.wagner@mcgill.ca.ORCID http://orcid.org/0000-0003-3794-1309
Hani N AlsafadiLund Stem Cell Center, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-1186-2517
Nilay MitashDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0001-8899-0915
Aurelien JustetPulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA.
Qianjiang HuDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0003-1069-3181
Ricardo PinedaDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.
Claudia Staab-WeijnitzInstitute for Lung Health and Immunity, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians Universität, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0002-1211-7834
Martina KorfeiDept of Internal Medicine, Justus-Liebig-Universität Giessen, Giessen, Germany.ORCID http://orcid.org/0000-0001-8177-2085
Nika GvazavaLund Stem Cell Center, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-8586-2192
Kristin WannemoDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0002-1457-3833
Ugochi OnwukaDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.
Molly MozurakDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.
Adriana Estrada-BernalDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0002-0555-2766
Juan Cala-GarciaDepartment of Internal Medicine. Yale University, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-2571-1373
Katrin MutzeLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0002-5577-4500
Rita CostaLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0003-0710-3611
Deniz BölükbasLund Stem Cell Center, Faculty of Medicine, Lund University, Lund, Sweden.
John StegmayrLund Stem Cell Center, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-8167-9259
Wioletta Skronska-WasekLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0001-7618-0034
Stephan KleeLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.
Chiharu OtaLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.
Hoeke A BaarsmaLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.
Jingtao WangMeakins-Christie Laboratories, Research-Institute of the McGill University Hospital, Montreal, QC, Canada.ORCID http://orcid.org/0000-0002-7552-8358
John SembratDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0003-4108-803X
Anne HilgendorffInstitute for Lung Health and Immunity, Helmholtz Zentrum München and University Hospital of the Ludwig Maximilians Universität, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0002-3725-996X
Jun DingMeakins-Christie Laboratories, Research-Institute of the McGill University Hospital, Montreal, QC, Canada.ORCID http://orcid.org/0000-0001-5183-6885
Andreas GüntherDept of Internal Medicine, Justus-Liebig-Universität Giessen, Giessen, Germany.ORCID http://orcid.org/0000-0002-2187-0975
Rachel ChambersCentre for Inflammation and Tissue Repair, UCL Respiratory, University College London, London, UK.ORCID http://orcid.org/0000-0003-1370-9417
Ivan RosasSection of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Stijn de LangheDepartment of Medicine, Division of Pulmonary and Critical Medicine, Mayo Clinic, Rochester, NY, USA.ORCID http://orcid.org/0000-0003-3867-4572
Naftali KaminskiPulmonary, Critical Care and Sleep Medicine, Yale School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0001-5917-4601
Mareike LehmannLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID http://orcid.org/0000-0002-8601-8206
Oliver EickelbergDivision of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine University of Pittsburgh, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0001-7170-0360
Melanie KönigshoffLung Repair and Regeneration Research Unit, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany. koenigshoffm@upmc.edu.ORCID http://orcid.org/0000-0001-9414-5128
Funding
TriState SenNET (Lung and Heart) Tissue Map and Atlas consortiumU54AG075931 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TOREN FINKEL, Melanie Koenigshoff · 2021 to 2026
$14.0MCell competition in pulmonary fibrosis and ARDSR35HL161169 · NHLBI · MAYO CLINIC ROCHESTER · PI Stijn Piet Johan De Langhe · 2022 to 2026
$4.7MExtracellular matrix composition and crosslinking patterns determine resident cell function in lung fibrosisR01HL146519 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI EICKELBERG, OLIVER · 2020 to 2023
$2.5MDeutsche Forschungsgemeinschaft (German Research Foundation) 512453064, BfR 60-0102-01.P588EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 805361NHLBI NIH HHS R01 HL146519NHLBI NIH HHS R35 HL161169NIA NIH HHS U54 AG075931Vetenskapsrådet (Swedish Research Council) 2018-02352
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease characterized by excessive extracellular matrix deposition. Current IPF therapies slow disease progression but do not stop or reverse it. The (myo)fibroblasts are thought to be the main cellular contributors to excessive extracellular matrix production in IPF. Here we show that fibrotic alveolar type II cells regulate production and crosslinking of extracellular matrix via the co-transcriptional activator YAP. YAP leads to increased expression of Lysl oxidase (LOX) and subsequent LOX-mediated crosslinking by fibrotic alveolar type II cells. Pharmacological YAP inhibition via verteporfin reverses fibrotic alveolar type II cell reprogramming and LOX expression in experimental lung fibrosis in vivo and in human fibrotic tissue ex vivo. We thus identify YAP-TEAD/LOX inhibition in alveolar type II cells as a promising potential therapy for IPF patients.
Indexed as
Adaptor Proteins, Signal TransducingDNA-Binding ProteinsIdiopathic Pulmonary FibrosisProtein-Lysine 6-OxidaseTranscription FactorsAlveolar Epithelial CellsAnimalsCell Cycle ProteinsDisease Models, AnimalExtracellular MatrixFemaleHumansLungMaleMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsProtein-Lysine 6-OxidaseTranscription FactorsVerteporfinYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins
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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 Socratic graph.