Search engine for discovering works of Art, research articles, and books related to Art and Culture
Javascript must be enabled to continue!
Role of C-Jun N terminal kinase (JNK) signaling pathway in acetaminophen hepatotoxicity
View through CrossRef
Acetaminophen (APAP) is a commonly used analgesics and antipyretic
agent. The therapeutic or recommended dose of APAP is not associated
with adverse effects. However, intentional or unintentional overdose of
APAP causes acute liver injury or acute liver failure if treatment is
delayed. Currently, APAP-induced liver injury is one of the major causes
of acute liver injury in the United States and other western countries.
C-Jun N terminal kinase (JNK) implicated in stress-related signaling
pathway plays an indispensable role in the mechanism of APAP
hepatotoxicity. JNK mediates depletion of mitochondrial glutathione in
the metabolic phase and enhances oxidative stress to aggravate liver
injury. In addition, JNK plays an important role in APAP-induced
apoptosis, necrosis or other forms of cell death. Furthermore, JNK plays
a role in regulation of endogenous immune system and aseptic
inflammatory responses induced by APAP. However, JNK may promote cell
regeneration after APAP-induced cell death. The present review therefore
highlights the functions of JNK in APAP-induced liver injury.
Title: Role of C-Jun N terminal kinase (JNK) signaling pathway in acetaminophen hepatotoxicity
Description:
Acetaminophen (APAP) is a commonly used analgesics and antipyretic
agent.
The therapeutic or recommended dose of APAP is not associated
with adverse effects.
However, intentional or unintentional overdose of
APAP causes acute liver injury or acute liver failure if treatment is
delayed.
Currently, APAP-induced liver injury is one of the major causes
of acute liver injury in the United States and other western countries.
C-Jun N terminal kinase (JNK) implicated in stress-related signaling
pathway plays an indispensable role in the mechanism of APAP
hepatotoxicity.
JNK mediates depletion of mitochondrial glutathione in
the metabolic phase and enhances oxidative stress to aggravate liver
injury.
In addition, JNK plays an important role in APAP-induced
apoptosis, necrosis or other forms of cell death.
Furthermore, JNK plays
a role in regulation of endogenous immune system and aseptic
inflammatory responses induced by APAP.
However, JNK may promote cell
regeneration after APAP-induced cell death.
The present review therefore
highlights the functions of JNK in APAP-induced liver injury.
Related Results
Role of C-Jun N terminal kinase (JNK) signaling pathway in acetaminophen hepatotoxicity
Role of C-Jun N terminal kinase (JNK) signaling pathway in acetaminophen hepatotoxicity
Acetaminophen (APAP) is a commonly used analgesics and antipyretic
agent. The therapeutic or recommended dose of APAP is not associated
with adverse effects. However, intentional o...
Increased Expression of Phosphorylated c-Jun Amino-terminal Kinase and Phosphorylated c-Jun in Human Cerebral Aneurysms: Role of the c-Jun Amino-terminal Kinase/c-Jun Pathway in Apoptosis of Vascular Walls
Increased Expression of Phosphorylated c-Jun Amino-terminal Kinase and Phosphorylated c-Jun in Human Cerebral Aneurysms: Role of the c-Jun Amino-terminal Kinase/c-Jun Pathway in Apoptosis of Vascular Walls
Abstract
OBJECTIVE
Vascular remodeling via apoptotic mechanisms is an important factor in vascular diseases. c-Jun amino-termina...
Cometary Physics Laboratory: spectrophotometric experiments
Cometary Physics Laboratory: spectrophotometric experiments
<p><strong><span dir="ltr" role="presentation">1. Introduction</span></strong&...
Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression
Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression
AbstractIn this study, we use an optogenetic inhibitor of c-Jun NH2-terminal kinase (JNK) in dendritic spine sub-compartments of rat hippocampal neurons. We show that JNK inhibitio...
Validation of ICD-9-CM/ICD-10 coding algorithms for the identification of patients with acetaminophen overdose and hepatotoxicity using administrative data
Validation of ICD-9-CM/ICD-10 coding algorithms for the identification of patients with acetaminophen overdose and hepatotoxicity using administrative data
Abstract
Background
Acetaminophen overdose is the most common cause of acute liver failure (ALF). Our objective was to develop coding algorithms usi...
ROLE OF HMGB1 IN DOXORUBICIN-INDUCED MYOCARDIAL APOPTOSIS AND ITS REGULATION PATHWAY
ROLE OF HMGB1 IN DOXORUBICIN-INDUCED MYOCARDIAL APOPTOSIS AND ITS REGULATION PATHWAY
Objectives
Doxorubicin (DOX) is a widely used anti-tumour agent. The clinical application of the medication is limited by its side effect which can elicit myocard...
Histopathological effects with marwar teak (tecomella undulata) bark extract and N-acetylcysteine on acetaminophen induced hepatotoxicity in albino rats.
Histopathological effects with marwar teak (tecomella undulata) bark extract and N-acetylcysteine on acetaminophen induced hepatotoxicity in albino rats.
Objective: The study aims to determine histopathological effects associated with Marwar Teak Tecomella Undulata bark extract and N-Acetylcysteine on Acetaminophen induced liver dam...
c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis
c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis
Osteoarthritis (OA) is a chronic degenerative joint disorder. Previous studies have shown abnormally increased apoptosis of chondrocytes in patients and animal models of OA. TNF-α ...