ArticleMedical science monitor : international medical journal of experimental and clinical research2011
Expression of angiotensinogen during hepatic fibrogenesis and its effect on hepatic stellate cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Lower circulating angiotensinogen levels across ACLD stages are associated with hepatic dysfunction and mortality.Hepatology communications · 2026Observational
- Unveiling the role of aldosterone in metabolic dysfunction-associated steatotic liver disease.Reviews in endocrine & metabolic disorders · 2026Review
- Liver Characterization of a Cohort of Alpha-1 Antitrypsin Deficiency Patients with and without Lung Disease.Journal of clinical and translational hepatology · 2024Article
- Genetic Polymorphism in Angiotensinogen and Its Association with Cardiometabolic Diseases.Metabolites · 2022Review
- Leukocyte cell-derived chemotaxin-2 and fibroblast growth factor 21 in alcohol-induced liver cirrhosis.World journal of hepatology · 2021Article
- Proteomic analysis of serum samples of paracoccidioidomycosis patients with severe pulmonary sequel.PLoS neglected tropical diseases · 2021Article
- Carvedilol Inhibits Angiotensin II-Induced Proliferation and Contraction in Hepatic Stellate Cells through the RhoA/Rho-Kinase Pathway.BioMed research international · 2019Article
- Balancing Effect of Biejiajian Oral Liquid () on ACE-Ang II-AT1R Axis and ACE2-Ang-(1-7)-Mas Axis in Rats with CClChinese journal of integrative medicine · 2018Article
- Exploring multiple quantitative trait loci models of hepatic fibrosis in a mouse intercross.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- MicroRNA-34a Promotes Hepatic Stellate Cell Activation via Targeting ACSL1.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- The BARD score and the NAFLD fibrosis score in the assessment of advanced liver fibrosis in nonalcoholic fatty liver disease.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- The effect of AVE 0991, nebivolol and doxycycline on inflammatory mediators in an apoE-knockout mouse model of atherosclerosis.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- Coexpression of Smad7 and UPA attenuates carbon tetrachloride-induced rat liver fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe liver renin-angiotensin system (RAS) plays an important role in promoting the development of hepatic fibrogenesis. Angiotensinogen (AGT) is an important precursor in tissue RAS. This study aimed to investigate the expression and cellular source of AGT in hepatic fibrogenesis and its effect on proliferation and collagen metabolism of hepatic stellate cells. MATERIAL/
methodsIn a rat carbon tetrachloride (CCl4)-induced liver fibrosis model the mRNA expression of AGT was determined by real-time PCR and the cellular source of AGT was determined by immunohistochemical staining. In vitro HSC-T6 cells were transfected with AGT, and the expression plasmid, AGT shRNA plasmid and negative shRNA plasmid were constructed. Real-time PCR and ELISA were applied to determine the mRNA expressions and contents of TIMP-1, TGF-β1, type I collagen and type III collagen of the cells or in the supernatants.
resultsCompared to normal liver, the AGT and α-SMA mRNA expressions increased at the early stage of hepatic fibrosis and decreased in hepatic cirrhosis. The expressions of AGT and α-SMA mRNA were correlated with the hepatic fibrosis (r=0.915, P=0.03). Immunohistochemistry demonstrated the activated HSCs were the main source of AGT due to colocalization of AGT and α-SMA expressions. The mRNA and protein of TGF-β1, TIMP-1, type I collagen and type III collagen were markedly up-regulated.
conclusionsACEI and angiotensin II type 1 receptor antagonist (AT1RA) could attenuate the progression of hepatic fibrosis in the early stage. Direct inhibition of AGT from aHSCs may become an effective antifibrotic anti-liver fibrosis strategy.
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