Epigenetics in Liver Fibrosis

2017 ◽  
Vol 37 (03) ◽  
pp. 219-230 ◽  
Author(s):  
Veronica Massey ◽  
Joaquin Cabezas ◽  
Ramon Bataller
Keyword(s):  
Dna Methylation ◽  
Liver Fibrosis ◽  
Epigenetic Regulation ◽  
Cell Activation ◽  
Stellate Cell ◽  
Epigenetic Mechanisms ◽  
Epigenetic Landscape ◽  
Chronic Liver Injury ◽  
Novel Biomarkers ◽  
Disease Specific

AbstractLiver fibrosis is a common consequence of chronic liver injury and is a key determinant of liver-associated morbidity and mortality. Identification of new mechanisms of fibrosis, including disease-specific molecular drivers, remains relevant to reveal novel biomarkers and therapeutic targets. Recently, greater accessibility to more advanced molecular methods that can assess changes in epigenetic regulation has stimulated more research investigating the epigenetic landscape of liver fibrosis. Such studies have revealed changes in DNA methylation, histone acetylation, and microRNAs that regulate the fibrogenic response to injury including hepatic stellate cell activation. The aim of this review is to briefly introduce the general mechanisms and epigenetic regulation of liver fibrosis and to familiarize the reader with the chief epigenetic mechanisms implicated as drivers of liver fibrosis.

scholarly journals Hepatic Stellate Cell–Macrophage Crosstalk in Liver Fibrosis and Carcinogenesis

2020 ◽  
Vol 40 (03) ◽  
pp. 307-320
Author(s):  
Michitaka Matsuda ◽  
Ekihiro Seki
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Cell Activation ◽  
Stellate Cell ◽  
Tumor Development ◽  
Mesenchymal Cell ◽  
Chronic Liver ◽  
Health Concern ◽  
Chronic Liver Injury ◽  
Fibrotic Liver

AbstractChronic liver injury due to viral hepatitis, alcohol abuse, and metabolic disorders is a worldwide health concern. Insufficient treatment of chronic liver injury leads to fibrosis, causing liver dysfunction and carcinogenesis. Most cases of hepatocellular carcinoma (HCC) develop in the fibrotic liver. Pathological features of liver fibrosis include extracellular matrix (ECM) accumulation, mesenchymal cell activation, immune deregulation, and angiogenesis, all of which contribute to the precancerous environment, supporting tumor development. Among liver cells, hepatic stellate cells (HSCs) and macrophages play critical roles in fibrosis and HCC. These two cell types interplay and remodel the ECM and immune microenvironment in the fibrotic liver. Once HCC develops, HCC-derived factors influence HSCs and macrophages to switch to protumorigenic cell populations, cancer-associated fibroblasts and tumor-associated macrophages, respectively. This review aims to summarize currently available data on the roles of HSCs and macrophages in liver fibrosis and HCC, with a focus on their interaction.

scholarly journals Induction of tropomyosin during hepatic stellate cell activation and the progression of liver fibrosis

2008 ◽  
Vol 3 (2) ◽  
pp. 378-383 ◽  
Author(s):  
Kohji Otogawa ◽  
Tomohiro Ogawa ◽  
Ryoko Shiga ◽  
Kazuo Ikeda ◽  
Norifumi Kawada
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Hepatic Stellate Cell Activation

scholarly journals The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masakazu Hanayama ◽  
Yasunori Yamamoto ◽  
Hiroki Utsunomiya ◽  
Osamu Yoshida ◽  
Shuang Liu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Portal Vein ◽  
Palmitic Acid ◽  
Intestinal Absorption ◽  
Nonalcoholic Steatohepatitis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Mrna Levels ◽  
Nonalcoholic Fatty Liver ◽  
Chylomicron Formation

AbstractDietary palmitic acid (PA) promotes liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). Herein, we clarified the intestinal absorption kinetics of dietary PA and effect of trans-portal PA on the activation of hepatic stellate cells (HSCs) involved in liver fibrosis in NASH. Blood PA levels after meals were significantly increased in patients with NASH compared to those in the control. Expression of genes associated with fat absorption and chylomicron formation, such as CD36 and MTP, was significantly increased in the intestine of NASH model rats compared with that in the controls. Plasma levels of glucagon-like peptide-2, involved in the upregulation of CD36 expression, were elevated in NASH rats compared with those in the controls. Furthermore, portal PA levels after meals in NASH rats were significantly higher than those in control and nonalcoholic fatty liver rats. Moreover, PA injection into the portal vein to the liver in control rats increased the mRNA levels associated with the activation of HSCs. Increased intestinal absorption of diet-derived PA was observed in NASH. Thus, the rapid increase in PA levels via the portal vein to the liver may activate HSCs and affect the development of liver fibrosis in NASH.

scholarly journals Dominant-negative soluble PDGF-β receptor inhibits hepatic stellate cell activation and attenuates liver fibrosis

2004 ◽  
Vol 84 (6) ◽  
pp. 766-777 ◽  
Author(s):  
Erawan Borkham-Kamphorst ◽  
Jens Herrmann ◽  
Doris Stoll ◽  
Jens Treptau ◽  
Axel M Gressner ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Dominant Negative ◽  
Hepatic Stellate Cell Activation ◽  
Β Receptor

scholarly journals Pro-fibrotic compounds induce stellate cell activation, ECM-remodelling and Nrf2 activation in a human 3D-multicellular model of liver fibrosis

PLoS ONE ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. e0179995 ◽  
Author(s):  
Vincenzo Prestigiacomo ◽  
Anna Weston ◽  
Simon Messner ◽  
Franziska Lampart ◽  
Laura Suter-Dick
Keyword(s):  
Liver Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Nrf2 Activation
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