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Matrix Metalloproteinases as Therapeutic Targets for Idiopathic Pulmonary Fibrosis
Open accessAbstract
Idiopathic pulmonary fibrosis (IPF) is a restrictive lung disease that is associated with high morbidity and mortality. Current medical therapies are not fully effective at limiting mortality in patients with IPF, and new therapies are urgently needed. Matrix metalloproteinases (MMPs) are proteinases that, together, can degrade all components of the extracellular matrix and numerous nonmatrix proteins. MMPs and their inhibitors, tissue inhibitors of MMPs (TIMPs), have been implicated in the pathogenesis of IPF based upon the results of clinical studies reporting elevated levels of MMPs (including MMP-1, MMP-7, MMP-8, and MMP-9) in IPF blood and/or lung samples. Surprisingly, studies of gene-targeted mice in murine models of pulmonary fibrosis (PF) have demonstrated that most MMPs promote (rather than inhibit) the development of PF and have identified diverse mechanisms involved. These mechanisms include MMPs: (1) promoting epithelial-to-mesenchymal transition (MMP-3 and MMP-7); (2) increasing lung levels or activity of profibrotic mediators or reducing lung levels of antifibrotic mediators (MMP-3, MMP-7, and MMP-8); (3) promoting abnormal epithelial cell migration and other aberrant repair processes (MMP-3 and MMP-9); (4) inducing the switching of lung macrophage phenotypes from M1 to M2 types (MMP-10 and MMP-28); and (5) promoting fibrocyte migration (MMP-8). Two MMPs, MMP-13 and MMP-19, have antifibrotic activities in murine models of PF, and two MMPs, MMP-1 and MMP-10, have the potential to limit fibrotic responses to injury. Herein, we review what is known about the contributions of MMPs and TIMPs to the pathogenesis of IPF and discuss their potential as therapeutic targets for IPF.
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“Inflammatory monocytes and tissue-resident macrophages are key regulators of tissue fibrosis, playing major roles in the initiation, maintenance and resolution of tissue injury58–60.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [59]
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Metadata
- Authors
- Craig, V. J., Zhang, L., Hagood, J. S., & Owen, C. A.
- Affiliations
- Brigham and Women's Hospital (US)
- University of California San Diego (US)
- Corresponding author
- Owen, Caroline A.
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-11-01
- Volume
- 53
- Issue
- 5
- Pages
- 585-600
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- PMC
- PMC4742954
- OpenAlex
- W1676246072
- Cited by
- 507
- References
- 210
- Citations by year
- 2026: 43 · 2025: 49 · 2024: 60 · 2023: 60 · 2022: 56 · 2021: 60 · 2020: 60 · 2019: 49 · 2018: 28 · 2017: 25 · 2016: 13 · 2015: 3
- FWCI
- 18.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Brigham and Women's Hospital
- U.S. Public Health Service (CIA123046)
- National Heart, Lung, and Blood Institute (HL114501, HL105339, R01HL086814, P01HL105339, AI111475-01, HL086814, R21HL111835, HL111835, HL063137, R01HL063137, T32HL007633, P01HL114501)
- National Institute of Allergy and Infectious Diseases (R01AI111475, AI111475‐01)
- National Institute of Environmental Health Sciences (P30ES007033)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Keywords
- idiopathic pulmonary fibrosis, matrix metalloproteinases, tissue inhibitors of metalloproteinases, MMP-3, MMP-7, MMP-8, MMP-9, MMP-13, MMP-19, epithelial-mesenchymal transition, macrophage polarization, extracellular matrix degradation, therapeutic target, antifibrotic mechanism
- MeSH terms
- Animals, Cell Movement, Disease Models, Animal, Extracellular Matrix, Gene Expression Regulation, Humans, Lung, Signal Transduction, Randomized Controlled Trials as Topic, Macrophages, Alveolar, Mice, Matrix Metalloproteinases, Secreted, Idiopathic Pulmonary Fibrosis, Epithelial-Mesenchymal Transition, Molecular Targeted Therapy, Matrix Metalloproteinase Inhibitors
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