ArticleInternational journal of biological sciences2018
Kupffer-derived matrix metalloproteinase-9 contributes to liver fibrosis resolution.
Article in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 103 citations in OpenAlex.
- Kaempferol Alleviates Aflatoxin B1-Induced Liver Injury by Mitigating Oxidative Stress.Nutrients · 2026Article
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- GSTM3 Knockdown Promotes Liver Fibrosis Reversal by Inhibiting Hepatic Stellate Cell Activation via PPARγ Signaling.Journal of clinical and translational hepatology · 2026Article
- The Matrix Reloaded: The Hepatic Matrisome as a Therapeutic Opportunity to Fight Liver Fibrosis.Biomolecules · 2026Review
- Cerium oxide nanoparticles attenuate hepatic failure via blocking TGF-β/Smads and upregulating Nrf2/HO-1 signaling pathways in liver fibrosis rat model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- RUNX2 enhances vascular remodeling to promote endothelial proliferation in acute liver injury.International journal of biological sciences · 2026Article
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- Immune System and Hepatic Stellate Cells' Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential.Journal of immunology research · 2026Review
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- Ferroptosis in liver fibrosis and its potential intervention strategy.Cell biology and toxicology · 2025Review
- Liver fibrosis with persistently normal alanine transaminase levels exhibits a distinct treatment response in MASLD.BMJ open gastroenterology · 2025Article
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- IQGAP1 participates in bone marrow-derived macrophage recruitment and involves in liver inflammation/fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- [CompoundNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Enolase and 16.5-kDa Tegument-Associated Protein inJournal of extracellular biology · 2025Article
- Role of triggering receptor expressed on myeloid cells 2 in the pathogenesis of non-alcoholic fatty liver disease.World journal of hepatology · 2025Review
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- TGF-β inhibitors: the future for prevention and treatment of liver fibrosis?Frontiers in immunology · 2025Review
- The possible protective effect of luteolin on cardiovascular and hepatic changes in metabolic syndrome rat model.Cell and tissue research · 2025Article
- Mouse Models for the Study of Liver Fibrosis RegressionJournal of clinical and translational hepatology · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kupffer cells (KCs) contribute to liver fibrosis resolution by production of a large spectrum of matrix metalloproteinases (MMPs). MMP9 is a major MMP expressed by KCs. However, its role in liver fibrosis resolution remains unclear. In this study, rodent liver fibrosis was induced by intraperitoneal thioacetamide (TAA) and the resolution process was initiated by TAA withdrawal. The role of KC-derived MMP9 in fibrolysis was investigated by adoptive transfer of KCs with or without MMP9 following their depletion. The levels of serum alanine aminotransferase (ALT) and hepatic cytokines were measured during fibrosis regression. The mRNA levels of MMPs and tissue inhibitor of metalloproteinases (TIMPs) were analyzed as well. It was found that removing KCs delayed fibrosis resolution. Adoptive transfer of KCs from WT animals promoted liver fibrosis resolution, compared with transfer of KCs from MMP9-/- mice. Depletion of KCs also resulted in prolonged liver wound healing, which was reversed partially by transferred KCs from either WT or MMP9-/- mice. Likewise, the absence of KCs led to reduction in MMPs mRNA levels and elevation in TIMPs mRNA levels. The expression patterns of MMPs or TIMPs were restored by adoptive transfer of the wild-type but not MMP9-/- KCs. In addition, liver fibrosis resolution was accelerated in MMP9-/- mice by adoptive transferred KCs from WT animals, compared to the KCs from MMP9-/- mice. Overall, KC-derived MMP9 plays a critical role in fibrosis resolution, which might serve as the foundation for developing anti-fibrosis therapy.
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