ArticleThe American journal of pathology2011
Matrix metalloproteinase 3 is a mediator of pulmonary fibrosis.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.
- A systematic review and network meta-analysis of single nucleotide polymorphisms associated with oral submucous fibrosis risk.Medicine · 2026Pooled it
- The BIOPREVENT machine-learning algorithm predicts chronic graft-versus-host disease and mortality risk using posttransplant biomarkers.The Journal of clinical investigation · 2026Trial
- Plasma matrix metalloproteinase-3 predicts mortality in acute respiratory distress syndrome: a biomarker analysis of a randomized controlled trial.Respiratory research · 2023Trial
- Computational Repurposing of FDA-Approved Drugs as Candidate MMP2 Inhibitors with Putative MMP3 Cross-Activity.International journal of molecular sciences · 2026Article
- Transcriptomics reveal dysregulated genes during folic acid-induced acute injury and fibrosis in kidney and their attenuation by antioxidantAmerican journal of physiology. Cell physiology · 2026Article
- Fibroblast activation protein inhibitor (FAPI) PET imaging in pulmonary fibrosis: pathophysiology, clinical utility, and emerging theranostic applications.Respiratory research · 2026Review
- Role of ADAMTS16 metalloproteinase in pathogenesis of cryptorchidism.Archives of medical science : AMS · 2026Article
- Exploring the role of PANoptosis in idiopathic pulmonary fibrosis based on scRNA-seq and bulk-seq.Clinical and experimental medicine · 2025Article
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- An Integrative Genotyping and Gene Expression Profiling of the Mutated Human FAM111B Gene and Fibrosis-Associated Pathway in the POIKTMP Syndrome.Journal of cellular and molecular medicine · 2025Article
- Potential biomarkers of idiopathic pulmonary fibrosis: metabonomics driven lipid profiling.Journal of translational medicine · 2025Article
- New therapeutic approaches for fibrosis: harnessing translational regulation.Trends in molecular medicine · 2025Review
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
- Combination therapy blocking TNF superfamily members 14 and 15 reverses pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The Intersection between Immune System and Idiopathic Pulmonary Fibrosis-A Concise Review.Fibrosis (Hong Kong, China) · 2025Article
- Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024Review
- Article
- Extracellular glucose triggers metabolic reprogramming of cultured human bronchial epithelial cells and indirect fibroblast activation.FEBS open bio · 2024Article
- MMP-3 mediates copper oxide nanoparticle-induced pulmonary inflammation and fibrosis.Journal of nanobiotechnology · 2024Article
- Review
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) may be triggered by epithelial injury that results in aberrant production of growth factors, cytokines, and proteinases, leading to proliferation of myofibroblasts, excess deposition of collagen, and destruction of the lung architecture. The precise mechanisms and key signaling mediators responsible for this aberrant repair process remain unclear. We assessed the importance of matrix metalloproteinase-3 (MMP-3) in the pathogenesis of IPF through i) determination of MMP-3 expression in patients with IPF, ii) in vivo experiments examining the relevance of MMP-3 in experimental models of fibrosis, and iii) in vitro experiments to elucidate possible mechanisms of action. Gene expression analysis, quantitative RT-PCR, and Western blot analysis of explanted human lungs revealed enhanced expression of MMP-3 in IPF, compared with control. Transient adenoviral vector-mediated expression of recombinant MMP-3 in rat lung resulted in accumulation of myofibroblasts and pulmonary fibrosis. Conversely, MMP-3-null mice were protected against bleomycin-induced pulmonary fibrosis. In vitro treatment of cultured lung epithelial cells with purified MMP-3 resulted in activation of the β-catenin signaling pathway, via cleavage of E-cadherin, and induction of epithelial-mesenchymal transition. These processes were inhibited in bleomycin-treated MMP-3-null mice, as assessed by cytosolic translocation of β-catenin and cyclin D1 expression. These observations support a novel role for MMP-3 in the pathogenesis of IPF, through activation of β-catenin signaling and induction of epithelial-mesenchymal transition.
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Registered trials
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.