ArticleInternational journal of molecular sciences2023
Amelioration of Pulmonary Fibrosis by Matrix Metalloproteinase-2 Overexpression.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Therapeutic Potential of Lentiviral miR-200a Mimics in Regulating Fibrinolysis and EMT Markers During Pulmonary Fibrosis.FASEB bioAdvances · 2026Article
- Bioresponsive gelatin-coated silk fibroin nanoparticles enhance roxadustat therapy in experimental pulmonary fibrosis.Frontiers in pharmacology · 2026Article
- Review
- Circulating biomarkers in patients with progressive fibrosing interstitial lung disease treated with nintedanib: a pilot study.Scientific reports · 2025Article
- What Is on the Horizon for Treatments in Idiopathic Pulmonary Fibrosis?Journal of clinical medicine · 2024Review
- Article
- Pathological mechanisms and novel drug targets in fibrotic interstitial lung disease.Inflammation and regeneration · 2024Review
- Zinc Iodide Dimethyl Sulfoxide Reduces Collagen Deposition by Increased Matrix Metalloproteinase-2 Expression and Activity in Lung Fibroblasts.Biomedicines · 2024Article
- Cell Death in Acute Organ Injury and Fibrosis.International journal of molecular sciences · 2024Article
- Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.Nature communications · 2024Article
- JTE-013 Alleviates Pulmonary Fibrosis by Affecting the RhoA/YAP Pathway and Mitochondrial Fusion/Fission.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Melatonin Modulates the SIRT1-Related Pathways via Transdermal Cryopass-Laser Administration in Prostate Tumor Xenograft.Cancers · 2023Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis is a progressive and fatal disease with a poor prognosis. Matrix metalloproteinase-2 is involved in the pathogenesis of organ fibrosis. The role of matrix metalloproteinase-2 in lung fibrosis is unclear. This study evaluated whether overexpression of matrix metalloproteinase-2 affects the development of pulmonary fibrosis. Lung fibrosis was induced by bleomycin in wild-type mice and transgenic mice overexpressing human matrix metalloproteinase-2. Mice expressing human matrix metalloproteinase-2 showed significantly decreased infiltration of inflammatory cells and inflammatory and fibrotic cytokines in the lungs compared to wild-type mice after induction of lung injury and fibrosis with bleomycin. The computed tomography score, Ashcroft score of fibrosis, and lung collagen deposition were significantly reduced in human matrix metalloproteinase transgenic mice compared to wild-type mice. The expression of anti-apoptotic genes was significantly increased, while caspase-3 activity was significantly reduced in the lungs of matrix metalloproteinase-2 transgenic mice compared to wild-type mice. Active matrix metalloproteinase-2 significantly decreased bleomycin-induced apoptosis in alveolar epithelial cells. Matrix metalloproteinase-2 appears to protect against pulmonary fibrosis by inhibiting apoptosis of lung epithelial cells.
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Registered trials
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