scholarly journals Integration of miRNA‐regulatory networks in hepatic stellate cells identifies TIMP3 as a key factor in chronic liver disease

2020 ◽  
Vol 40 (8) ◽  
pp. 2021-2033 ◽  
Author(s):  
Fida Azar ◽  
Kevin Courtet ◽  
Bassil Dekky ◽  
Dominique Bonnier ◽  
Olivier Dameron ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Stellate Cells ◽  
Regulatory Networks ◽  
Stellate Cells ◽  
Chronic Liver ◽  
Key Factor

scholarly journals Activated Hepatic Stellate Cells Express Keratinocyte Growth Factor in Chronic Liver Disease

2004 ◽  
Vol 165 (4) ◽  
pp. 1233-1241 ◽  
Author(s):  
Heike Steiling ◽  
Marcus Mühlbauer ◽  
Frauke Bataille ◽  
Jürgen Schölmerich ◽  
Sabine Werner ◽  
...  
Keyword(s):  
Liver Disease ◽  
Growth Factor ◽  
Chronic Liver Disease ◽  
Hepatic Stellate Cells ◽  
Keratinocyte Growth Factor ◽  
Stellate Cells ◽  
Chronic Liver ◽  
Activated Hepatic Stellate Cells

scholarly journals Differential TM4SF5-mediated SIRT1 modulation and signaling for chronic liver disease

2020 ◽  
Author(s):  
Jihye Ryu ◽  
Eunmi Kim ◽  
Min-Kyung Kang ◽  
Dae-Geun Song ◽  
Eun-Ae Shin ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Liver Damage ◽  
Hepatic Stellate Cells ◽  
Lipid Accumulation ◽  
Stellate Cells ◽  
Dependent Manner ◽  
Fibrosis Score ◽  
Age Dependent

AbstractHere we show the roles of transmembrane 4 L six family member 5 (TM4SF5) in the progression of nonalcoholic steatosis (or NAFL) to steatohepatitis (NASH). The overexpression of TM4SF5 caused nonalcoholic steatosis and NASH in an age-dependent manner. Initially, TM4SF5-positive hepatocytes and livers exhibited lipid accumulation, decreased SIRT1, increased SREBPs levels, and inactive STAT3 via SOCS1/3 upregulation. In older animals, TM4SF5 under an inflammatory environment increased SIRT1 expression and STAT3 activity with no significant change to SOCSs and SREBPs levels, leading to active STAT3-mediated fibrotic extracellular matrix (ECM) production. Liver tissues from clinical human patients with NAFL or NASH also showed such a TM4SF5-SIRT1-STAT3-ECM relationship correlated with fibrosis score and age. Ligand-independent and TM4SF5-mediated STAT3 activity led to collagen I and laminins/laminin γ2 expression in hepatic stellate cells and hepatocytes, respectively. Laminin γ2 suppression abolished CCl4-mediated liver damage and ECM production and reduced SIRT1 and active-STAT3, but did not alter SREBP1 or SOCSs levels. These findings suggest that TM4SF5, CCL20, SIRT1, and/or laminin γ2 may be promising therapeutic targets against liver disease.

Genetic predictors of spontaneous viral elimination or chronic liver disease in hepatitis C infection

2001 ◽  
Vol 120 (5) ◽  
pp. A7-A7
Author(s):  
S ROSS ◽  
S MASCHERETTI ◽  
H HINRICHSEN ◽  
P BUGGISCH ◽  
U FOELSCH ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Hepatitis C Infection ◽  
Genetic Predictors
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