ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- Causal effects of circulating inflammatory proteins on COPD: A Mendelian randomization study.Medicine · 2026Article
- A retrospective analysis of the anatomic characteristics of pulmonary bullae based on chest CT classification and their association with pulmonary function.Frontiers in medicine · 2026Article
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway.International journal of chronic obstructive pulmonary disease · 2026Article
- The bronchoalveolar proteome changes in obesity.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Reversing VTN deficiency inhibits the progression of pancreatic cancer and enhances sensitivity to anti-PD1 immunotherapy.Frontiers in immunology · 2025Article
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Authors and funding
25 authors.
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Abstract
Vitronectin (VTN) is an important extracellular matrix protein in tissue remodeling, but its role in chronic obstructive pulmonary disease (COPD) is unknown. We show that VTN regulates tissue remodeling through urokinase plasminogen activator (uPA) signaling pathway in COPD. In human COPD airways and bronchoepithelial cells and the airways of mice with cigarette smoke (CS)-induced experimental COPD, VTN protein was not changed, but downstream uPA signaling was altered (increased plasminogen activator inhibitor-1) that induced collagen and airway remodeling. In the parenchyma, VTN levels were decreased, uPA signaling pathway differentially altered and collagen reduced in lung fibroblasts from human and lung parenchyma in experimental COPD. Vtn inhibition with siRNA in mouse fibroblasts altered uPA signaling increased matrix metalloproteinase-12, and reduced collagen, whereas over-expression restored collagen production after CS extract challenge. Vtn
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