Mitochondrial dysfunction in hepatitis C virus infection.
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: