Electron leak from NDUFA13 within mitochondrial complex I attenuates ischemia-reperfusion injury via dimerized STAT3

@article{Hu2017ElectronLF,
  title={Electron leak from NDUFA13 within mitochondrial complex I attenuates ischemia-reperfusion injury via dimerized STAT3},
  author={Hengxun Hu and J. Nan and Yong Sun and Danyan Zhu and Changchen Xiao and Yaping Wang and Lianlian Zhu and Yue Wu and J. Zhao and R. Wu and Jinghai Chen and Hong Yu and Xinyang Hu and W. Zhu and Jian’an Wang},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2017},
  volume={114},
  pages={11908 - 11913}
}
  • Hengxun Hu, J. Nan, +12 authors Jian’an Wang
  • Published 2017
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
Significance Reactive oxygen species (ROS) generation due to electron leak from the mitochondria may be involved in physiological or pathological processes. NDUFA13 is an accessory subunit of mitochondria complex I with a unique molecular structure and is located close to FeS clusters with low electrochemical potentials. Here, we generated cardiac-specific conditional NDUFA13 heterozygous knockout mice. At the basal state, a moderate down-regulation of NDUFA13 created a leak within complex I… Expand
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