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

Novo E, Parola M - Fibrogenesis Tissue Repair (2012)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Experimental Medicine and Oncology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy ; Interuniversity Centre for Liver Pathophysiology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Major antioxidant defences in mammalian cells. A brief overview of antioxidant defences is offered. Antioxidant defences have been subdivided in those having as a major goal to display protection versus ROS and other oxidants (left panels) and in those (including both naturally occurring and synthetic molecules) able to prevent the chain reactions of lipid peroxidation (right panels).
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Figure 2: Major antioxidant defences in mammalian cells. A brief overview of antioxidant defences is offered. Antioxidant defences have been subdivided in those having as a major goal to display protection versus ROS and other oxidants (left panels) and in those (including both naturally occurring and synthetic molecules) able to prevent the chain reactions of lipid peroxidation (right panels).

Mentions: Aerobic organisms use molecular oxygen (O2) as the final electron acceptor for mitochondrial cytochrome c oxidase that, as terminal functional element of mitochondrial NADH dehydrogenase enzyme complex, catalyzes the four electron reduction of O2 [1]. During mitochondrial oxidative phosphorylation and other electron transfer reactions partially reduced and highly reactive oxygenspecies (ROS) are generated, including superoxide anion (O2•-), hydrogen peroxide (H2O2) and hydroxyl radical (•OH), that at very high levels can result in cell injury and death, according to their properties and intracellular sources (resumed in Figure 1). In order to survive, aerobic organisms have developed evolutionary conserved mechanisms and strategies (including antioxidant defences resumed in Figure 2, see ref. [5] for more details) to carefully control generation of ROS and other oxidative stress - related mediators to maintain intracellular redox homeostasis and to use these reactive intermediates to modulate signal transduction, gene expression and cellular responses (i.e., redox signaling) [1-5]. At present, it is widely accepted that increased and/or sustained levels of ROS and other mediators of oxidative stress play a significant role in atherosclerosis, diabetes, cardiovascular diseases, cancer, neuro-degenerative diseases as well as in chronic inflammatory and fibrogenic diseases involving chronic activation of wound healing, including chronic liver and lung diseases.


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

Novo E, Parola M - Fibrogenesis Tissue Repair (2012)

Major antioxidant defences in mammalian cells. A brief overview of antioxidant defences is offered. Antioxidant defences have been subdivided in those having as a major goal to display protection versus ROS and other oxidants (left panels) and in those (including both naturally occurring and synthetic molecules) able to prevent the chain reactions of lipid peroxidation (right panels).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368756&req=5

Figure 2: Major antioxidant defences in mammalian cells. A brief overview of antioxidant defences is offered. Antioxidant defences have been subdivided in those having as a major goal to display protection versus ROS and other oxidants (left panels) and in those (including both naturally occurring and synthetic molecules) able to prevent the chain reactions of lipid peroxidation (right panels).
Mentions: Aerobic organisms use molecular oxygen (O2) as the final electron acceptor for mitochondrial cytochrome c oxidase that, as terminal functional element of mitochondrial NADH dehydrogenase enzyme complex, catalyzes the four electron reduction of O2 [1]. During mitochondrial oxidative phosphorylation and other electron transfer reactions partially reduced and highly reactive oxygenspecies (ROS) are generated, including superoxide anion (O2•-), hydrogen peroxide (H2O2) and hydroxyl radical (•OH), that at very high levels can result in cell injury and death, according to their properties and intracellular sources (resumed in Figure 1). In order to survive, aerobic organisms have developed evolutionary conserved mechanisms and strategies (including antioxidant defences resumed in Figure 2, see ref. [5] for more details) to carefully control generation of ROS and other oxidative stress - related mediators to maintain intracellular redox homeostasis and to use these reactive intermediates to modulate signal transduction, gene expression and cellular responses (i.e., redox signaling) [1-5]. At present, it is widely accepted that increased and/or sustained levels of ROS and other mediators of oxidative stress play a significant role in atherosclerosis, diabetes, cardiovascular diseases, cancer, neuro-degenerative diseases as well as in chronic inflammatory and fibrogenic diseases involving chronic activation of wound healing, including chronic liver and lung diseases.

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Experimental Medicine and Oncology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy ; Interuniversity Centre for Liver Pathophysiology, University of Torino, Corso Raffaello 30, 10125, Torino, Italy.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus