Abstract
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 mtΔΨ, 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1429-1437 |
| Number of pages | 9 |
| Journal | Biochimica et Biophysica Acta - Bioenergetics |
| Volume | 1757 |
| Issue number | 9-10 |
| DOIs | |
| Publication status | Published - Sep 2006 |
Fingerprint
Keywords
- Calcium
- Complex I
- Endoplasmic reticulum
- HCV
- Inducible gene expression
- Mitochondria
- Reactive oxygen specie
ASJC Scopus subject areas
- Biophysics
Cite this
Mitochondrial dysfunction in hepatitis C virus infection. / Piccoli, C.; Scrima, R.; D'Aprile, A.; Ripoli, M.; Lecce, L.; Boffoli, D.; Capitanio, N.
In: Biochimica et Biophysica Acta - Bioenergetics, Vol. 1757, No. 9-10, 09.2006, p. 1429-1437.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mitochondrial dysfunction in hepatitis C virus infection
AU - Piccoli, C.
AU - Scrima, R.
AU - D'Aprile, A.
AU - Ripoli, M.
AU - Lecce, L.
AU - Boffoli, D.
AU - Capitanio, N.
PY - 2006/9
Y1 - 2006/9
N2 - 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 mtΔΨ, 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.
AB - 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 mtΔΨ, 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.
KW - Calcium
KW - Complex I
KW - Endoplasmic reticulum
KW - HCV
KW - Inducible gene expression
KW - Mitochondria
KW - Reactive oxygen specie
UR - http://www.scopus.com/inward/record.url?scp=33748958673&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33748958673&partnerID=8YFLogxK
U2 - 10.1016/j.bbabio.2006.05.018
DO - 10.1016/j.bbabio.2006.05.018
M3 - Article
C2 - 16814246
AN - SCOPUS:33748958673
VL - 1757
SP - 1429
EP - 1437
JO - Biochimica et Biophysica Acta - Bioenergetics
JF - Biochimica et Biophysica Acta - Bioenergetics
SN - 0005-2728
IS - 9-10
ER -