Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24040957
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Antioxid+Redox+Signal
2014 ; 20
(17
): 2854-72
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Role of NADPH oxidases in liver fibrosis
#MMPMID24040957
Paik YH
; Kim J
; Aoyama T
; De Minicis S
; Bataller R
; Brenner DA
Antioxid Redox Signal
2014[Jun]; 20
(17
): 2854-72
PMID24040957
show ga
SIGNIFICANCE: Hepatic fibrosis is the common pathophysiologic process resulting
from chronic liver injury, characterized by the accumulation of an excessive
extracellular matrix. Multiple lines of evidence indicate that oxidative stress
plays a pivotal role in the pathogenesis of liver fibrosis. Nicotinamide adenine
dinucleotide phosphate (NADPH) oxidase (NOX) is a multicomponent enzyme complex
that generates reactive oxygen species (ROS) in response to a wide range of
stimuli. In addition to phagocytic NOX2, there are six nonphagocytic NOX
proteins. RECENT ADVANCES: In the liver, NOX is functionally expressed both in
the phagocytic form and in the nonphagocytic form. NOX-derived ROS contributes to
various kinds of liver disease caused by alcohol, hepatitis C virus, and toxic
bile acids. Recent evidence indicates that both phagocytic NOX2 and nonphagocytic
NOX isoforms, including NOX1 and NOX4, mediate distinct profibrogenic actions in
hepatic stellate cells, the main fibrogenic cell type in the liver. The critical
role of NOX in hepatic fibrogenesis provides a rationale to assess
pharmacological NOX inhibitors that treat hepatic fibrosis in patients with
chronic liver disease. CRITICAL ISSUES: Although there is compelling evidence
indicating a crucial role for NOX-mediated ROS generation in hepatic
fibrogenesis, little is known about the expression, subcellular localization,
regulation, and redox signaling of NOX isoforms in specific cell types in the
liver. Moreover, the exact mechanism of NOX-mediated fibrogenic signaling is
still largely unknown. FUTURE DIRECTIONS: A better understanding through further
research about NOX-mediated fibrogenic signaling may enable the development of
novel anti-fibrotic therapy using NOX inhibition strategy. Antio
free
free
free
