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Mitochondrial dysfunction in hepatitis C virus infection.
Piccoli, C; Scrima, R; D'Aprile, A; Ripoli, M; Lecce, L; Boffoli, D; Capitanio, N.
Affiliation
  • Piccoli C; Department of Biomedical Science, University of Foggia, viale L. Pinto OO.RR. 71100 Foggia, Italy.
Biochim Biophys Acta ; 1757(9-10): 1429-37, 2006.
Article in En | MEDLINE | ID: mdl-16814246
The mechanisms of liver injury in chronic hepatitis C virus (HCV) infection are poorly understood though HCV induces a state of hepatic oxidative stress that is more pronounced than that present in many other inflammatory diseases. This mini-review will focus on recent findings revealing an unexpected role of mitochondria in providing a central role in the innate immunity and in addition will illustrate the application of stably transfected human-derived cell lines, inducibly expressing the entire HCV open reading frame for in vitro studies on mitochondria. Results obtained by a comparative analysis of the respiratory chain complexes activities along with mitochondrial morpho-functional confocal microscopy imaging show a detrimental effect of HCV proteins on the cell oxidative metabolism with specific inhibition of complex I activity, decrease of mtDeltaPsi, increased production of reactive oxygen species. A possible de-regulation of calcium recycling between the endoplasmic reticulum and the mitochondrial network is discussed to provide new insights in the pathogenesis of hepatitis C.
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Collection: 01-internacional Database: MEDLINE Main subject: Hepatitis C / Mitochondrial Diseases / Mitochondria Limits: Humans Language: En Journal: Biochim Biophys Acta Year: 2006 Document type: Article Affiliation country: Country of publication:
Search on Google
Collection: 01-internacional Database: MEDLINE Main subject: Hepatitis C / Mitochondrial Diseases / Mitochondria Limits: Humans Language: En Journal: Biochim Biophys Acta Year: 2006 Document type: Article Affiliation country: Country of publication: