scholarly journals NADPH Oxidases in Chronic Liver Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Joy X. Jiang ◽  
Natalie J. Török
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Liver Diseases ◽  
Wide Spectrum ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Chronic Liver ◽  
Cellular Distribution ◽  
Oxygen Species ◽  
Chronic Liver Diseases ◽  
Nadph Oxidases ◽  
Regulatory Pathways

Oxidative stress is a common feature observed in a wide spectrum of chronic liver diseases including viral hepatitis, alcoholic, and nonalcoholic steatohepatitis. The nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are emerging as major sources of reactive oxygen species (ROS). Several major isoforms are expressed in the liver, including NOX1, NOX2, and NOX4. While the phagocytic NOX2 has been known to play an important role in Kupffer cell and neutrophil phagocytic activity and inflammation, the nonphagocytic NOX homologues are increasingly recognized as key enzymes in oxidative injury and wound healing. In this review, we will summarize the current advances in knowledge on the regulatory pathways of NOX activation, their cellular distribution, and their role in the modulation of redox signaling in liver diseases.

scholarly journals Mitochondrial Roles and Cytoprotection in Chronic Liver Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Davide Degli Esposti ◽  
Jocelyne Hamelin ◽  
Nelly Bosselut ◽  
Raphaël Saffroy ◽  
Mylène Sebagh ◽  
...  
Keyword(s):  
Liver Diseases ◽  
Hepatic Metabolism ◽  
Chronic Liver ◽  
Oxygen Species ◽  
Organelle Biogenesis ◽  
Chronic Liver Diseases ◽  
Chronic Liver Injury ◽  
Promising Therapeutic Target ◽  
Apoptosis And Necrosis

The liver is one of the richest organs in terms of number and density of mitochondria. Most chronic liver diseases are associated with the accumulation of damaged mitochondria. Hepatic mitochondria have unique features compared to other organs' mitochondria, since they are the hub that integrates hepatic metabolism of carbohydrates, lipids and proteins. Mitochondria are also essential in hepatocyte survival as mediator of apoptosis and necrosis. Hepatocytes have developed different mechanisms to keep mitochondrial integrity or to prevent the effects of mitochondrial lesions, in particular regulating organelle biogenesis and degradation. In this paper, we will focus on the role of mitochondria in liver physiology, such as hepatic metabolism, reactive oxygen species homeostasis and cell survival. We will also focus on chronic liver pathologies, especially those linked to alcohol, virus, drugs or metabolic syndrome and we will discuss how mitochondria could provide a promising therapeutic target in these contexts.

scholarly journals Propofol Reduces Lipopolysaccharide-Induced, NADPH Oxidase (NOX2) Mediated TNF-αand IL-6 Production in Macrophages

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Tao Meng ◽  
Jingya Yu ◽  
Zhen Lei ◽  
Jianbo Wu ◽  
Shuqin Wang ◽  
...  
Keyword(s):  
Nicotinamide Adenine Dinucleotide ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Immunomodulatory Activity ◽  
Ros Production ◽  
Oxygen Species ◽  
Murine Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Nadph Oxidases ◽  
Lps Signaling

During an infection, lipopolysaccharide (LPS) stimulates the production of reactive oxygen species (ROS), which is mediated, in large part, by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs); NOX2is the major NOX isoform found in the macrophage cell membrane. While the immunomodulatory activity of propofol is highly documented, its effect on the LPS-induced NOX2/ROS/NF-κB signaling pathway in macrophages has not been addressed. In present study, we used murine macrophage cell line RAW264.7 pretreated with propofol and stimulated with LPS. IL-6 and TNF-αexpression, ROS production, and NOX activity were determined. Results showed that propofol attenuated LPS-induced TNF-αand IL-6 expression. Moreover, LPS-stimulated phosphorylation of NF-κB and generation of ROS were weakened in response to propofol. Propofol also reduced LPS-induced NOX activity and expression of gp91phox and p47phox. We conclude that propofol modulates LPS signaling in macrophages by reducing NOX-mediated production of TNF-αand IL-6.

Helicobacter infection in patients with HCV-chronic liver diseases

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

TRAF1-C5as risk locus for increased hepatic fibrosis in chronic liver diseases

2008 ◽  
Vol 46 (09) ◽  
Author(s):  
F Grünhage ◽  
A Höblinger ◽  
S Schwartz ◽  
T Sauerbruch ◽  
F Lammert
Keyword(s):  
Hepatic Fibrosis ◽  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Risk Locus

Targeting TGF-β2 in chronic liver diseases

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

Role of scavenger receptors in the pathophysiology of chronic liver diseases

2013 ◽  
Author(s):  
Carolina Armengol ◽  
Ramon Bartoli ◽  
Lucia Sanjurjo ◽  
Isabel Serra ◽  
Nuria Amezaga ◽  
...  
Keyword(s):  
Liver Diseases ◽  
Chronic Liver ◽  
Scavenger Receptors ◽  
Chronic Liver Diseases

The Connection between Hypercoagulability and Fibrogenesis in Chronic Liver Diseases

2020 ◽  
Vol 25 (5) ◽  
pp. 1851-1860
Author(s):  
ROMEO-GABRIEL MIHĂILĂ ◽  
◽  
ADRIAN BOICEAN ◽  
VICTORIA BÎRLUȚIU
Keyword(s):  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases
Sign in / Sign up

Export Citation Format

Share Document