Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10796031 | Biochimica et Biophysica Acta (BBA) - Bioenergetics | 2009 | 8 Pages |
Abstract
Cells infected by the hepatitis C virus (HCV) are characterized by endoplasmic reticulum stress, deregulation of the calcium homeostasis and unbalance of the oxido-reduction state. In this context, mitochondrial dysfunction proved to be involved and is thought to contribute to the outcome of the HCV-related disease. 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 causes successive mitochondrial alterations comprising generation of reactive oxygen and nitrogen species and impairment of the oxidative phosphorylation. A progressive adaptive response results in an enhancement of the glycolytic metabolism sustained by up-regulation of the hypoxia inducible factor. Pathogenetic implications of the model are discussed.
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Authors
C. Piccoli, G. Quarato, M. Ripoli, A. D'Aprile, R. Scrima, O. Cela, D. Boffoli, D. Moradpour, N. Capitanio,