The DOI matches its Crossref record; 212 of the 212 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis
Richeldi, L., du Bois, R. M., Raghu, G., Azuma, A., Brown, K. K., Costabel, U., Cottin, V., Flaherty, K. R., Hansell, D. M., Inoue, Y., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1402584 · Cited by 4,654
A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis.
King, T. E., Bradford, W. Z., Castro-Bernardini, S., Fagan, E. A., Glaspole, I., Glassberg, M. K., Gorina, E., Hopkins, P. M., Kardatzke, D., Lancaster, L., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1402582 · Cited by 3,975
Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis
Bergers, G., Brekken, R., McMahon, G., Vu, T. H., Itoh, T., Tamaki, K., Tanzawa, K., Thorpe, P., Itohara, S., Werb, Z., et al. (2000) · Nature Cell Biology · doi:10.1038/35036374 · Cited by 2,797
Matrix Metalloproteinase Inhibitors and Cancer—Trials and Tribulations
Coussens, L. M., Fingleton, B., & Matrisian, L. M. (2002) · Science · doi:10.1126/science.1067100 · Cited by 2,761
A matrix metalloproteinase expressed on the surface of invasive tumour cells
Sato, H., Takino, T., Okada, Y., Cao, J. P., Shinagawa, A., Yamamoto, E., & Seiki, M. (1994) · Nature · doi:10.1038/370061a0 · Cited by 2,534
Mechanism Of Cell Surface Activation Of 72-kDa Type IV Collagenase
Strongin, A. Y., Collier, I. E., Bannikov, G. A., Marmer, B. L., Grant, G. A., & Goldberg, G. I. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.10.5331 · Cited by 1,589
Regulation of matrix metalloproteinase expression in tumor invasion
Westermarck, J. K., & Kähäri, V. (1999) · The FASEB Journal · doi:10.1096/fasebj.13.8.781 · Cited by 1,494
Van Wart, H. E., & Birkedal-Hansen, H. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.14.5578 · Cited by 1,475
Holmbeck, K., Bianco, P., Caterina, J., Yamada, S., Kromer, M., Kuznetsov, S. A., Mankani, M., Gehron Robey, P., Poole, A. R., Pidoux, I., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80064-1 · Cited by 1,298
Regulation of matrix metalloproteinases: An overview
Chakraborti, S., Mandal, M., Das, S. K., Mandal, A., & Chakraborti, T. (2003) · Molecular and Cellular Biochemistry · doi:10.1023/a:1026028303196 · Cited by 1,123
Flagged first, then by citations
Cited by
Sorted by citations
Items 501–507 of 507
Yang, Y., 刘森玉, Wang, S., Zhang, A., Wang, W., Zhu, Z., Zhang, X., & Liu, X. (2026) · Pharmacological Research · doi:10.1016/j.phrs.2026.108437
Chae, H., Valappil, A. K., Kang, I.-H., Jung, N., Shin, H., Kim, J., Kwon, M., Kim, J.-H., Hong, S.-U., Ryu, M., et al. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.116027
Li, L., Chu, P., Kao, W. W. ‐., Yu, C.-C., Huang, C.-Y., Wu, H.-P., Chu, C., Liu, P., & Liu, Y.-Y. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27198515
Padureanu, M. M., MARINESCU, I., Mitroi, D. M., Coanda, R. M., Roșu, S.-M., Stoica, A. S., Pomacu, M. M., Stan, S. I., Croitoru, A., Bănicioiu-Covei, S., et al. (2026) · Frontiers in Medicine · doi:10.3389/fmed.2026.1930150
Tomos, I. P., Spathis, A., Argentos, S., Karakatsani, A., Manali, E. D., & Papiris, S. A. (2026) · Therapeutic Advances in Respiratory Disease · doi:10.1177/17534666261493434
Niu, W., Hu, G., Xie, S., Wang, Y., Zhang, Z., Liu, Y., Shen, H., Xuan, J., Xia, J., Zheng, Q., et al. (2026) · Current Pharmaceutical Analysis · doi:10.1016/j.cpan.2026.10.008
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
