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Updated: Jul 13, 2026
15:43
Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
Published on: January 7, 2013
Hepatitis C virus protein expression causes calcium-mediated mitochondrial bioenergetic dysfunction and
Claudia Piccoli1, Rosella Scrima, Giovanni Quarato
1Department of Biomedical Sciences, University of Foggia, Foggia, Italy.
Hepatology (Baltimore, Md.)
|June 15, 2007
Summary
Hepatitis C virus (HCV) protein expression disrupts cell energy production by impairing mitochondrial function. This viral effect is linked to calcium imbalance, offering potential therapeutic targets for hepatitis C.
Area of Science:
- Hepatology
- Virology
- Cellular Metabolism
Background:
- Hepatitis C virus (HCV) infection causes significant oxidative stress.
- Understanding HCV's impact on cellular bioenergetics is crucial for disease insight.
Purpose of the Study:
- To investigate how HCV protein expression affects cellular bioenergetics.
- To elucidate the role of mitochondrial dysfunction in HCV pathogenesis.
Main Methods:
- Utilized cell lines inducibly expressing the full HCV open-reading frame.
- Assessed mitochondrial function, including complex I activity, membrane potential, and oxidative phosphorylation.
- Investigated the role of mitochondrial calcium uptake in bioenergetic alterations.
Main Results:
- HCV protein expression inhibited mitochondrial complex I activity and reduced membrane potential.
- Observed decreased oxidative phosphorylation coupling efficiency and loss of the Pasteur effect.
- Demonstrated that mitochondrial calcium overload is causally linked to these bioenergetic defects.
Conclusions:
- HCV protein expression disrupts mitochondrial calcium homeostasis, preceding other mitochondrial dysfunctions.
- This calcium deregulation leads to altered bioenergetic balance and nitro-oxidative stress.
- Findings offer new insights into hepatitis C pathogenesis and potential therapeutic strategies targeting mitochondrial function.
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