Hepatic Fibrosis

Bataller, Ramón; Brenner, David A.

doi:10.1002/9780470747919.ch29

Cited by 9 publications

(12 citation statements)

References 181 publications

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“…HSC/MF and, likely, all MFs are target cells for inflammatory cytokines and other pro-inflammatory signals like (a) ROS and other oxidative stress-related mediators like 4-hydroxy-2,3-nonenal or HNE, generated as a consequence of hepatocyte injury and necrosis, (b) apoptotic bodies (engulfing and activating), and (c) bacterial endotoxin or other endogenous activators of Toll Like Receptor 4 (TLR4) of innate immunity displayed by HSC/MFs. On the other hand, HSC/MFs are also the cell source (even in an autocrine manner) of a number of pro-inflammatory molecules, including TLR ligands, MCP-1 and other chemoattractants and chemokines (Bataller andBrenner, 2005 andFriedman, 2008b). HSC/MFs can also play a crucial role in modulating hepatic immune responses (reviewed in Friedman, 2008a andFriedman, 2008b), and then fibrogenesis, by behaving as antigen presenting cells, by inducing locally immunotolerance throughout T cell suppression or by interacting directly with subsets of T lymphocytes (mainly CD8).…”

Section: Hsc/mfs In Inflammatory Signalling and Regulation Of Immune ...mentioning

confidence: 99%

Hepatic myofibroblasts: A heterogeneous population of multifunctional cells in liver fibrogenesis

Novo

Bonzo

Cannito

et al. 2009

The International Journal of Biochemistry & Cell Biology

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Section: Hsc/mfs In Inflammatory Signalling and Regulation Of Immune ...mentioning

confidence: 99%

Hepatic myofibroblasts: A heterogeneous population of multifunctional cells in liver fibrogenesis

Novo

Bonzo

Cannito

et al. 2009

The International Journal of Biochemistry & Cell Biology

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“…The most common causes of liver fibrosis are viral hepatitis C or B, alcohol abuse, schistosomiasis, and nonalcoholic fatty liver disease (NAFLD) [3] . Yet, it still remains unclear whether the genetic factors aggravate the formation and development of liver fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Association between TM6SF2 rs58542926 T/C gene polymorphism and significant liver fibrosis: A meta-analysis

Mei

Zhang

Tang

et al. 2020

Preprint

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Aim: To further explore the association between Transmembrane 6 superfamily member 2(TM6SF2) rs58542926 T/C gene polymorphism and hepatic fibrosis. Materials and Methods: In this study the MEDLINE, PubMed, EMBASE, and CENTRAL databases were queried from inception to March 21, 2020. According to inclusion and exclusion criteria; case control studies assessing the relationship between TM6SF2 rs58542926 T/C gene polymorphism and significant liver fibrosis were selected. NOS scale was used to evaluate the included literature. Stata 12.0 software was used for data analysis. Results: In this meta analysis: a total of 7 articles, including 2286 patients were included. Statistical analysis showed that the TM6SF2 gene polymorphism was associated with significant liver fibrosis in the allele contrast, recessive dominant models (T vs. C, OR=1.292, 95%CI 1.035-1.611, P=0.023; TT vs. CT+CC, OR=2.829, 95%CI 1.101-7.267, P=0.031). No significant publication bias was found after Egger′s test.

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“…Table ( 8) shows that there's no significant difference in the comparison between responders to interferon therapy and non responders as regarding PCR by using Mann Whitney test. Table (9) illustrates that serum TNF-alpha was ( 79.3) in patients and was (52) in the controls. Table (10) shows that serum TNF-alpha was higher among CHCV patients as compared to controls with statistically highly significant difference in between by using unpaired ttest.…”

Section: Methodsmentioning

confidence: 98%

“…TNF-α and IFN-γ were upregulated in chronic HCV infection (8). Baller et al (9) noticed that polymorphisms in genes encoding immunoregulatory proteins, proinflammatory cytokines, and fibrogenic factors may affect the production of these factors and influence disease progression in patients with chronic liver disease due to alcohol, primary biliary cirrhosis or hepatitis C. Polymorphisms in the promoter of the TNF-α gene have been reported to affect the transcription rate and the release of this cytokine (10). The G-A transition at positions -308 and -238, have been shown to influence TNF-α expression (11,12).…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor-Alpha ( TNF-α ) Gene Expression in Chronic Hepatitis B Virus Infection

Farid

Sweilam

Rashed

et al. 2015

EJHM

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Objective: Tumour necrosis factor (TNF)-alpha, a prototype proinflammatory cytokine, has been implicated as an important pathogenic mediator in a variety of liver conditions. Some genetic polymorphisms in the human TNF-alpha promoter region, such as the G-A transitions-308 and-238, have been shown to influence TNF-alpha expression in chronic hepatitis C virus infection. Aim of the work: The present study was to investigate the influence that the-308 and-238 TNF-alpha promoter polymorphisms have on the response to interferon and ribavirin therapy in chronic hepatitis C virus infection. Patients and methods: One hundred forty patients with chronic hepatitis C virus infection, their age ranges between (20-56) years, selected from the National Hepatology and Tropical Medicine Research Institute were included in this study, during interferon and ribavirin therapy and thirty five healthy individuals were included to serve as controls, the patients and controls were divided into two groups the first group forty patients and fifteen controls for the detection of TNF-alpha-308,-238 genotypes polymorphisms, the second group were one hundred patients and twenty healthy controls for the detection of serum levels of TNF-α. All the patients and controls were subjected to the following history, clinical examination, abdominal ultrasonography and collection of blood samples for routine laboratory investigation, CBCs and serological assay, genotyping of 308, 238 TNF-alpha promoter polymorphism and serum levels of TNF-α. Results: There was no statistically significant difference between chronic HCV patients and healthy controls as regarding TNF-alpha-238 different alleles. The frequencies of TNF-alpha gene polymorphism with A/G and G/G mutation at-308 were significantly higher in chronic HCV patients than those in the controls. The serum level of TNF-alpha was markedly higher in the chronic HCV patients than in the healthy controls. There were significant association between TNF-alpha gene polymorphism in the-308 A/G, G/G alleles and increased serum TNF-alpha in CHCV infection. Conclusion: The results indicate that the TNF-alpha gene polymorphism at position-308 is associated with susceptibility of chronic HCV infection. Recommendations: Our major concern was to improve the response to treatment in patients with chronic HCV infection, whether the disadvantage of having the TNF-alpha-308 allele became more apparent after interferon and ribavirin therapy is unclear and needs further study that detecting the polymorphism of the-308 TNF-alpha allele before administering interferon therapy may be valuable for predicting the treatment response, especially in difficult-to treat patients.

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Hepatic Fibrosis

Cited by 9 publications

References 181 publications

Hepatic myofibroblasts: A heterogeneous population of multifunctional cells in liver fibrogenesis

Hepatic myofibroblasts: A heterogeneous population of multifunctional cells in liver fibrogenesis

Association between TM6SF2 rs58542926 T/C gene polymorphism and significant liver fibrosis: A meta-analysis

Tumor Necrosis Factor-Alpha ( TNF-α ) Gene Expression in Chronic Hepatitis B Virus Infection

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