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- W2023654566 endingPage "166" @default.
- W2023654566 startingPage "156" @default.
- W2023654566 abstract "Hepatitis C virus (HCV) infection induces a state of oxidative stress more pronounced than that observed in many other inflammatory diseases. Here, we propose a temporal sequence of events in the HCV-infected cell whereby the primary alteration consists of a release of Ca2+ from the endoplasmic reticulum, followed by uptake into mitochondria. This ensues successive mitochondrial dysfunction leading to the generation of reactive oxygen species and a progressive metabolic adaptive response. Evidence is provided for a positive feed-back mechanism between alterations of calcium and redox homeostasis. This likely involves deregulation of the mitochondrial permeability transition and induces progressive dysfunction of cellular bioenergetics. Pathogenetic implications of the model and new opportunities for therapeutic intervention are discussed. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy." @default.
- W2023654566 created "2016-06-24" @default.
- W2023654566 creator A5008558621 @default.
- W2023654566 creator A5031763741 @default.
- W2023654566 creator A5039786016 @default.
- W2023654566 creator A5046309539 @default.
- W2023654566 creator A5060005797 @default.
- W2023654566 creator A5091273319 @default.
- W2023654566 date "2013-01-01" @default.
- W2023654566 modified "2023-10-15" @default.
- W2023654566 title "Targeting mitochondria in the infection strategy of the hepatitis C virus" @default.
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