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- W2800340823 abstract "Oxidative stress is a reflection of the imbalance between the production of reactive oxygen species (ROS) and the scavenging capacity of the antioxidant system. Excessive ROS, generated from various endogenous oxidative biochemical enzymes, interferes with the normal function of liver-specific cells and presumably plays a role in the pathogenesis of liver fibrosis. Once exposed to harmful stimuli, Kupffer cells (KC) are the main effectors responsible for the generation of ROS, which consequently affect hepatic stellate cells (HSC) and hepatocytes. ROS-activated HSC undergo a phenotypic switch and deposit an excessive amount of extracellular matrix that alters the normal liver architecture and negatively affects liver function. Additionally, ROS stimulate necrosis and apoptosis of hepatocytes, which causes liver injury and leads to the progression of end-stage liver disease. In this review, we overview the role of ROS in liver fibrosis and discuss the promising therapeutic interventions related to oxidative stress. Most importantly, novel drugs that directly target the molecular pathways responsible for ROS generation, namely, mitochondrial dysfunction inhibitors, endoplasmic reticulum stress inhibitors, NADPH oxidase (NOX) inhibitors, and Toll-like receptor (TLR)-affecting agents, are reviewed in detail. In addition, challenges for targeting oxidative stress in the management of liver fibrosis are discussed." @default.
- W2800340823 created "2018-05-17" @default.
- W2800340823 creator A5023853436 @default.
- W2800340823 creator A5024496478 @default.
- W2800340823 creator A5026115044 @default.
- W2800340823 creator A5062954228 @default.
- W2800340823 creator A5078818670 @default.
- W2800340823 creator A5080856061 @default.
- W2800340823 date "2018-01-01" @default.
- W2800340823 modified "2023-10-14" @default.
- W2800340823 title "Targeting Oxidative Stress for the Treatment of Liver Fibrosis" @default.
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