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Redox Biology and Liver Fibrosis
Summary
This review explores how disrupted redox balance in the liver contributes to the development and progression of hepatic fibrosis across various chronic liver diseases. Researchers describe how persistent damage to liver cells triggers overproduction of reactive species, which in turn activate specific signaling pathways that drive scar tissue formation. The study identifies several redox-dependent pathways as potential therapeutic targets for slowing or preventing liver fibrosis.
Hepatic fibrosis is a complex process that develops in chronic liver diseases. Even though the initiation and progression of fibrosis rely on the underlying etiology, mutual mechanisms can be recognized and targeted for therapeutic purposes. Irrespective of the primary cause of liver disease, persistent damage to parenchymal cells triggers the overproduction of reactive species, with the consequent disruption of redox balance. Reactive species are important mediators for the homeostasis of both hepatocytes and non-parenchymal liver cells. Indeed, other than acting as cytotoxic agents, reactive species are able to modulate specific signaling pathways that may be relevant to hepatic fibrogenesis. After a brief introduction to redox biology and the mechanisms of fibrogenesis, this review aims to summarize the current evidence of the involvement of redox-dependent pathways in liver fibrosis and focuses on possible therapeutic targets.
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