In EXOG-depleted cardiomyocytes cell death is marked by a decreased mitochondrial reserve capacity of the electron transport chain.

@article{Tigchelaar2016InEC,
  title={In EXOG-depleted cardiomyocytes cell death is marked by a decreased mitochondrial reserve capacity of the electron transport chain.},
  author={Wardit Tigchelaar and Anne Margreet de Jong and Wiek H van Gilst and Rudolf A de Boer and Herman H W Sillj{\'e}},
  journal={BioEssays : news and reviews in molecular, cellular and developmental biology},
  year={2016},
  volume={38 Suppl 1},
  pages={S136-45}
}
Depletion of mitochondrial endo/exonuclease G-like (EXOG) in cultured neonatal cardiomyocytes stimulates mitochondrial oxygen consumption rate (OCR) and induces hypertrophy via reactive oxygen species (ROS). Here, we show that neurohormonal stress triggers cell death in endo/exonuclease G-like-depleted cells, and this is marked by a decrease in… CONTINUE READING