IGFBP-3: So Much More Than an IGF1/2 Binding Protein
| Autor: | Montserrat Marí |
|---|---|
| Přispěvatelé: | Instituto de Salud Carlos III, European Commission, Marí, Montserrat [0000-0002-6116-3247], Marí, Montserrat |
| Rok vydání: | 2020 |
| Předmět: |
Liver Cirrhosis
0301 basic medicine bp base pair Economic growth Integrin Signaling EZH enhancer of zeste homologue Epigenesis Genetic Histones Mice 0302 clinical medicine Cell Movement Transforming Growth Factor beta CCl4 carbon tetrachloride Insulin-Like Growth Factor I Phosphorylation Cells Cultured Migration media_common Original Research Mice Knockout TGF-β transforming growth factor β PDGFR platelet-derived growth factor receptor Integrin beta1 Gastroenterology Acetylation ELISA enzyme-linked immunosorbent assay GIPC HSC hepatic stellate cell mRNA messenger RNA Up-Regulation AKT Protein Kinase B H3K27 histone 3 lysine K27 Editorial Work (electrical) Liver WB Western blot GAPDH glyceraldehyde-3-phosphate dehydrogenase Gene Knockdown Techniques qPCR quantitative polymerase chain reaction 030211 gastroenterology & hepatology ChIP chromatin-immunoprecipitation Signal Transduction Primary Cell Culture European Regional Development Fund BDL bile duct ligation chr chromosome 03 medical and health sciences IGFBP-3 insulin-like growth factor binding protein-3 Political science Hypertension Portal Hepatic Stellate Cells Animals media_common.cataloged_instance Humans hg human genome browse lcsh:RC799-869 European union Adaptor Proteins Signal Transducing Hepatology Binding protein IGFBP-3 LSEC liver sinusoidal endothelial cells Fibrosis WT wild-type Disease Models Animal 030104 developmental biology Insulin-Like Growth Factor Binding Protein 3 αSMA α–smooth muscle actin siRNA small interfering RNA lcsh:Diseases of the digestive system. Gastroenterology Biomarkers |
| Zdroj: | Cellular and Molecular Gastroenterology and Hepatology Digital.CSIC. Repositorio Institucional del CSIC instname Cellular and Molecular Gastroenterology and Hepatology, Vol 10, Iss 3, Pp 643-644 (2020) |
| ISSN: | 2352-345X |
| Popis: | Portal hypertension is a major consequence of the progression of chronic liver disease, leading to high morbidity and mortality.1 The prognosis of patients with portal hypertension has improved dramatically in the past decades mainly owing to a better understanding of its pathogenesis and the discovery of new therapeutic targets. An uncontrolled increase in intrahepatic vascular resistance, derived from the profound deregulation in the phenotype of all hepatic cell types, is the primary factor in the development of portal hypertension.2 During continuous hepatic injury, hepatic stellate cells (HSCs) acquire proliferative, procontractile, and procollagen–synthetic properties, which together with the increased extracellular matrix deposition results in enhanced vascular tone and augmented liver stiffness. Therefore, fibrosis remains the principal cause of increased vascular resistance in liver disease. Because HSCs are involved in both fibrosis and portal hypertension, HSC targeting is considered in the prevention and treatment of complications of chronic liver disease This work was supported by the Instituto de Salud Carlos III Project PI19/01410 and co-funded by European Union (European Regional Development Fund A way to make Europe). |
| Databáze: | OpenAIRE |
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