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Cited by 102Liver physiology and pathologyLiver Diseases and ImmunityLiver Disease Diagnosis and Treatment

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

PAI‐1 deficiency reduces liver fibrosis after bile duct ligation in mice through activation of tPA

Wang, Hongtao, Zhang, Yan, Heuckeroth, Robert O.·2007·FEBS Letters
DOI 10.1016/j.febslet.2007.05.049
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Abstract

Plasminogen activator inhibitor‐1 (PAI‐1) increases injury in several liver, lung and kidney disease models. The objective of this investigation was to assess the effect of PAI‐1 deficiency on cholestatic liver fibrosis and determine PAI‐1 influenced fibrogenic mechanisms. We found that PAI‐1 −/− mice had less fibrosis than wild type (WT) mice after bile duct ligation. This change correlated with increased tissue‐type plasminogen activator (tPA) activity, and increased matrix metalloproteinase‐9 (MMP‐9), but not MMP‐2 activity. Furthermore, there was increased activation of the tPA substrate hepatocyte growth factor (HGF), a known anti‐fibrogenic protein. In contrast, there was no difference in hepatic urokinase plasminogen activator (uPA) or plasmin activities between PAI‐1 −/− and WT mice. There was also no difference in the level of transforming growth factor beta 1 (TGF‐β1), stellate cell activation or collagen production between WT and PAI‐1 −/− animals. In conclusion, PAI‐1 deficiency reduces hepatic fibrosis after bile duct obstruction mainly through the activation of tPA and HGF.

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Crossref · 10.1016/j.febslet.2007.05.049

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  1. Kaibori M., 2002, The role of biologically active HGF, Hepatology, 34, 475
  2. 10.1097/00005176-199807000-00013 · DOI
  3. 10.1016/j.thromres.2004.12.019 · DOI

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Metadata

Authors
Wang, H., Zhang, Y., & Heuckeroth, R. O.
Affiliations
  • Washington University in St. Louis (US)
  • Sun Yat-sen University (CN)
Corresponding author
Heuckeroth, Robert O.
ORCID
Venue
FEBS Letters
Publisher
Wiley
Published
2007-05-29
Volume
581
Issue
16
Pages
3098-3104
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
DOI
10.1016/j.febslet.2007.05.049
OpenAlex
W1970138640
Cited by
98
References
35
Citations by year
2026: 4 · 2025: 8 · 2024: 4 · 2023: 2 · 2022: 4 · 2021: 7 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 8 · 2016: 4 · 2015: 3 · 2014: 7 · 2013: 9 · 2012: 5
FWCI
3.65
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • FEBS Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1c06rr015502-01)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 068371, P30 DK-52574, R01DK064592, DK 64592, DK62452, R01DK057038, R21DK068371, DK57038, U01DK062452, P30DK056341, P30DK052574)
  • National Center for Research Resources (C06-RR-015502)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
  • Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Keywords
plasminogen activator inhibitor-1, liver fibrosis, bile duct ligation, cholestasis, tissue plasminogen activator, hepatocyte growth factor, MMP-9, urokinase, plasmin, hepatic stellate cells, TGF-β1
MeSH terms
Animals, Bile Ducts, Fibrinolysin, Ligation, Liver, Liver Cirrhosis, Male, Mice, Inbred C57BL, Tissue Plasminogen Activator, Urokinase-Type Plasminogen Activator, Hepatocyte Growth Factor, Plasminogen Activator Inhibitor 1, Mice, Knockout, Matrix Metalloproteinase 9, Mice, Transforming Growth Factor beta1

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