Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress.

@article{Griffiths2010ElectronTC,
  title={Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress.},
  author={Eric R Griffiths and Ingeborg Friehs and Elisabeth Scherr and Dimitrios N. Poutias and Francis X. McGowan and Pedro J. del Nido},
  journal={The Journal of thoracic and cardiovascular surgery},
  year={2010},
  volume={139 6},
  pages={1609-17}
}
OBJECTIVES We have previously shown in a model of pressure-overload hypertrophy that there is increased cardiomyocyte apoptosis during the transition from peak hypertrophy to ventricular decompensation. Electron transport chain dysfunction is believed to play a role in this process through the production of excessive reactive oxygen species. In this study we sought to determine electron transport chain function in pressure-overload hypertrophy and the role of oxidative stress in myocyte… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 11 extracted citations

Selective downregulation of mitochondrial electron transport chain activity and increased oxidative stress in human atrial fibrillation.

American journal of physiology. Heart and circulatory physiology • 2016
View 4 Excerpts
Highly Influenced

References

Publications referenced by this paper.
Showing 1-10 of 32 references

Domestication of the cardiac mitochondrion for energy conversion.

Journal of molecular and cellular cardiology • 2009
View 1 Excerpt

Energy metabolism in heart failure and remodelling.

Cardiovascular research • 2009
View 1 Excerpt

Similar Papers

Loading similar papers…