ArticleArchives of medical science : AMS2015
Blockade of CCN4 attenuates CCl4-induced liver fibrosis.
Article in Archives of medical science : AMS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Lysophosphatidic acid mediates skeletal muscle fibrosis in denervation via activation of YAP/TAZ.JCI insight · 2026Article
- Turmeric-derived exosome-coated ZIF-8 nanoplatform for targeted delivery of TGF-β1 siRNA in the treatment of liver fibrosis.Journal of nanobiotechnology · 2026Article
- Promising impacts ofBiochemistry and biophysics reports · 2025Review
- Article
- An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024Review
- Injectable Peptide Hydrogels Loaded with Murine Embryonic Stem Cells Relieve IschemiaBiomacromolecules · 2024Article
- Recent progress on the role of cellular communication network factors (CCN) 3, 4 and 6 in regulating adiposity, liver fibrosis and pancreatic islets.Journal of cell communication and signaling · 2023Review
- Significance of CCNs in liver regeneration.Journal of cell communication and signaling · 2023Review
- Expression and biological function of the cellular communication network factor 5 (CCN5) in primary liver cells.Journal of cell communication and signaling · 2023Article
- C6orf120 gene deficiency may be vulnerable to carbon tetrachloride induced acute hepatic injury in rats.Archives of medical science : AMS · 2022Article
- Matricellular Protein WISP2 Is an Endogenous Inhibitor of Collagen Linearization and Cancer Metastasis.Cancer research · 2021Article
- Article
- The Emerging Roles of CCN3 Protein in Immune-Related Diseases.Mediators of inflammation · 2021Review
- Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020Review
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- Thermodynamic Aspects and Reprogramming Cellular Energy Metabolism during the Fibrosis Process.International journal of molecular sciences · 2017Review
- Interactions between TGF-β1, canonical WNT/β-catenin pathway and PPAR γ in radiation-induced fibrosis.Oncotarget · 2017Review
- Tissue expression of β-catenin and E- and N-cadherins in chronic hepatitis C and hepatocellular carcinoma.Archives of medical science : AMS · 2017Article
- Serum levels of WNT1-inducible signaling pathway protein-1 (WISP-1): a noninvasive biomarker of renal fibrosis in subjects with chronic kidney disease.American journal of translational research · 2017Article
- Members of the Cyr61/CTGF/NOV Protein Family: Emerging Players in Hepatic Progenitor Cell Activation and Intrahepatic Cholangiocarcinoma.Gastroenterology research and practice · 2016Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCCN4, also termed WNT-inducible signaling pathway protein-1 (WISP-1), has important roles in inflammation and tissue injury. This study aimed to investigate the effect of CCN4 inhibition using monoclonal anti-CCN4 antibody (CCN4mAb) on the liver injury and fibrosis in a mouse model of liver fibrosis. MATERIAL AND
methodsThe mouse liver fibrosis model was induced by carbon tetrachloride (CCl4). Mice received vehicle (saline/olive oil) by subcutaneous injection, CCl4 by subcutaneous injection or CCl4 (subcutaneous) plus CCN4mAb by subcutaneous injection. The pro-inflammatory and pro-fibrotic factors were determined by Western blot. The biochemistry and histopathology, collagen deposition and nuclear factor (NF)-κB activity were also assessed.
resultsChronic CCl4 treatment caused liver injury and collagen accumulation. The expression levels of CCN4, pro-inflammatory and pro-fibrotic mediators as well as the activity of NF-κB were markedly increased. Treatment with CCN4mAb significantly inhibited CCl4-induced CCN4 expression, leading to attenuated CCl4-induced liver injury and the inflammatory response. CCN4 blockade also significantly reduced the formation of collagen in the liver and the expression of α-smooth muscle actin and transforming growth factor β1.
conclusionsCCN4 inhibition by CCN4mAb in vivo significantly attenuated the CCl4-induced liver injury and the progression of liver fibrosis. CCN4 may represent a novel therapeutic target for liver injury and fibrosis.
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