ArticlePloS one2012
Hepatoprotective effect of MMP-19 deficiency in a mouse model of chronic liver fibrosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Expression profiles of lncRNAs and their possible regulatory role in monocrotaline-induced HSOS in rats.Frontiers in genetics · 2023Article
- ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis.Scientific reports · 2021Article
- Transcriptional regulation of alcohol induced liver fibrosis in a translational porcine hepatocellular carcinoma model.Biochimie · 2021Article
- Noninvasive Assessment of Liver Fibrosis: Current and Future Clinical and Molecular Perspectives.International journal of molecular sciences · 2020Review
- Matrix Metalloproteinases as Potential Biomarkers and Therapeutic Targets in Liver Diseases.Cells · 2020Review
- Resolution of organ fibrosis.The Journal of clinical investigation · 2018Review
- Matrix Metalloproteinases (MMPs) in Liver Diseases.Journal of clinical and experimental hepatology · 2017Review
- Adenoviral‑bone morphogenetic protein‑7 and/or doxazosin therapies promote the reversion of fibrosis/cirrhosis in a cirrhotic hamster model.Molecular medicine reports · 2017Article
- Drugs and Targets in Fibrosis.Frontiers in pharmacology · 2017Review
- Biochemical and Biological Attributes of Matrix Metalloproteinases.Progress in molecular biology and translational science · 2017Review
- Matrix Metalloproteinases in Non-Neoplastic Disorders.International journal of molecular sciences · 2016Review
- MMP-19 deficiency causes aggravation of colitis due to defects in innate immune cell function.Mucosal immunology · 2016Article
- Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2015Review
- Diverse functions of matrix metalloproteinases during fibrosis.Disease models & mechanisms · 2014Review
- Liver protective effect of ursodeoxycholic acid includes regulation of ADAM17 activity.BMC gastroenterology · 2013Article
- Matrix metalloproteinases in liver injury, repair and fibrosis.Matrix biology : journal of the International Society for Matrix BiologyReview
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is characterized by the deposition and increased turnover of extracellular matrix. This process is controlled by matrix metalloproteinases (MMPs), whose expression and activity dynamically change during injury progression. MMP-19, one of the most widely expressed MMPs, is highly expressed in liver; however, its contribution to liver pathology is unknown. The aim of this study was to elucidate the role of MMP-19 during the development and resolution of fibrosis by comparing the response of MMP-19-deficient (MMP19KO) and wild-type mice upon chronic liver CCl(4)-intoxication. We show that loss of MMP-19 was beneficial during liver injury, as plasma ALT and AST levels, deposition of fibrillar collagen, and phosphorylation of SMAD3, a TGF-ß1 signaling molecule, were all significantly lower in MMP19KO mice. The ameliorated course of the disease in MMP19KO mice likely results from a slower rate of basement membrane destruction and ECM remodeling as the knockout mice maintained significantly higher levels of type IV collagen and lower expression and activation of MMP-2 after 4 weeks of CCl(4)-intoxication. Hastened liver regeneration in MMP19KO mice was associated with slightly higher IGF-1 mRNA expression, slightly increased phosphorylation of Akt kinase, decreased TGF-ß1 mRNA levels and significantly reduced SMAD3 phosphorylation. In addition, primary hepatocytes isolated from MMP19KO mice showed impaired responsiveness towards TGF-ß1 stimulation, resulting in lower expression of Snail1 and vimentin mRNA. Thus, MMP-19-deficiency improves the development of hepatic fibrosis through the diminished replacement of physiological extracellular matrix with fibrotic deposits in the beginning of the injury, leading to subsequent changes in TGF-ß and IGF-1 signaling pathways.
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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.