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This article is part of the supplement: Proceedings of Fibroproliferative disorders: from biochemical analysis to targeted therapies

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The role of redox mechanisms in hepatic chronic wound healing and fibrogenesis

Erica Novo12 and Maurizio Parola12*

Author Affiliations

1 Department of Experimental Medicine and Oncology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy

2 Interuniversity Centre for Liver Pathophysiology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy

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Fibrogenesis & Tissue Repair 2012, 5(Suppl 1):S4  doi:10.1186/1755-1536-5-S1-S4

Published: 6 June 2012


Under physiological conditions, intracellular and tissue levels of reactive oxygen species (ROS) are carefully controlled and employed as fine modulators of signal transduction, gene expression and cell functional responses (redox signaling). A significant derangement in redox homeostasis, resulting in sustained levels of oxidative stress and related mediators, plays a role in the pathogenesis of human diseases characterized by chronic inflammation, chronic activation of wound healing and tissue fibrogenesis, including chronic liver diseases. In this chapter major concepts and mechanisms in redox signaling will be briefly recalled to introduce a number of selected examples of redox-related mechanisms that can actively contribute to critical events in the natural history of a chronic liver diseases, including induction of cell death, perpetuation of chronic inflammatory responses and fibrogenesis. A major focus will be on redox-dependent mechanisms involved in the modulation of phenotypic responses of activated, myofibroblast-like, hepatic stellate cells (HSC/MFs), still considered as the most relevant pro-fibrogenic cells operating in chronic liver diseases.