scholarly journals Interactions between Myc and Mediators of Inflammation in Chronic Liver Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ting Liu ◽  
Yu Zhou ◽  
Kwang Suk Ko ◽  
Heping Yang

Most chronic liver diseases (CLDs) are characterized by inflammatory processes with aberrant expressions of various pro- and anti-inflammatory mediators in the liver. These mediators are the driving force of many inflammatory liver disorders, which often result in fibrosis, cirrhosis, and liver tumorigenesis. c-Myc is involved in many cellular events such as cell growth, proliferation, and differentiation. c-Myc upregulates IL-8, IL-10, TNF-α, and TGF-β, while IL-1, IL-2, IL-4, TNF-α, and TGF-βpromote c-Myc expression. Their interactions play a central role in fibrosis, cirrhosis, and liver cancer. Molecular interference of their interactions offers possible therapeutic potential for CLDs. In this review, current knowledge of the molecular interactions between c-Myc and various well known inflammatory mediators is discussed.

2017 ◽  
Vol 6 (3) ◽  
pp. 280-289 ◽  
Author(s):  
Aniruddha Adhikari ◽  
Nabarun Polley ◽  
Soumendra Darbar ◽  
Samir Kumar Pal

Gut ◽  
2020 ◽  
Vol 69 (5) ◽  
pp. 953-962 ◽  
Author(s):  
Jaime Bosch ◽  
Jordi Gracia-Sancho ◽  
Juan G Abraldes

In the recent years, there have been an increasing number of reports on favourable effects of statins in patients with advanced chronic liver disease. These include reduction in portal pressure, improved liver sinusoidal endothelial and hepatic microvascular dysfunction, decreased fibrogenesis, protection against ischaemia/reperfusion injury, safe prolongation of ex vivo liver graft preservation, reduced sensitivity to endotoxin-mediated liver damage, protection from acute-on-chronic liver failure, prevention of liver injury following hypovolaemic shock and preventing/delaying progression of cirrhosis of any aetiology. Moreover, statins have been shown to have potential beneficial effects in the progression of other liver diseases, such as chronic sclerosing cholangitis and in preventing hepatocellular carcinoma. Because of these many theoretically favourable effects, statins have evolved from being considered a risk to kind of wonder drugs for patients with chronic liver diseases. The present article reviews the current knowledge on the potential applications of statins in chronic liver diseases, from its mechanistic background to objective evidence from clinical studies.


2016 ◽  
Vol 130 (23) ◽  
pp. 2121-2138 ◽  
Author(s):  
Guillermo Mazzolini ◽  
Jan-Peter Sowa ◽  
Ali Canbay

The liver is constantly exposed to a host of injurious stimuli. This results in hepatocellular death mainly by apoptosis and necrosis, but also due to autophagy, necroptosis, pyroptosis and in some cases by an intricately balanced combination thereof. Overwhelming and continuous cell death in the liver leads to inflammation, fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Although data from various disease models may suggest a specific (predominant) cell death mode for different aetiologies, the clinical reality is not as clear cut. Reliable and non-invasive cell death markers are not available in general practice and assessment of cell death mode to absolute certainty from liver biopsies does not seem feasible, yet. Various aetiologies probably induce different predominant cell death modes within the liver, although the death modes involved may change during disease progression. Moreover, current methods applicable in patients are limited to surrogate markers for apoptosis (M30), and possibly for pyroptosis (IL-1 family) and necro(pto)sis (HMGB1). Although markers for some death modes are not available at all (autophagy), others may not be specific for a cell death mode or might not always definitely indicate dying cells. Physicians need to take care in asserting the presence of cell death. Still the serum-derived markers are valuable tools to assess severity of chronic liver diseases. This review gives a short overview of known hepatocellular cell death modes in various aetiologies of chronic liver disease. Also the limitations of current knowledge in human settings and utilization of surrogate markers for disease assessment are summarized.


2001 ◽  
Vol 120 (5) ◽  
pp. A725-A725
Author(s):  
M DORE ◽  
G REALDI ◽  
D MURA ◽  
D GRAHAM ◽  
A SEPULVEDA

2008 ◽  
Vol 46 (09) ◽  
Author(s):  
F Grünhage ◽  
A Höblinger ◽  
S Schwartz ◽  
T Sauerbruch ◽  
F Lammert

2015 ◽  
Vol 53 (01) ◽  
Author(s):  
A Dropmann ◽  
H Korhonen ◽  
F Jaschinski ◽  
M Janicot ◽  
N Meindl-Beinker ◽  
...  

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