Ameliorating Endothelial Mitochondrial Dysfunction Restores Coronary Function via Transient Receptor Potential Vanilloid 1-Mediated Protein Kinase A/Uncoupling Protein 2 Pathway.

@article{Xiong2016AmelioratingEM,
  title={Ameliorating Endothelial Mitochondrial Dysfunction Restores Coronary Function via Transient Receptor Potential Vanilloid 1-Mediated Protein Kinase A/Uncoupling Protein 2 Pathway.},
  author={Shiqiang Xiong and Peijian Wang and Liqun Ma and P. P. Gao and Liuping Gong and Li Li and Qiang Hua Li and Fang Sun and Xunmei Zhou and Hongbo He and Jing Chen and Zhencheng Yan and Daoyan Liu and Zhiming Zhu},
  journal={Hypertension},
  year={2016},
  volume={67 2},
  pages={451-60}
}
Coronary heart disease arising from atherosclerosis is a leading cause of cardiogenic death worldwide. Mitochondria are the principal source of reactive oxygen species (ROS), and defective oxidative phosphorylation by the mitochondrial respiratory chain contributes to ROS generation. Uncoupling protein 2 (UCP2), an adaptive antioxidant defense factor, protects against mitochondrial ROS-induced endothelial dysfunction in atherosclerosis. The activation of transient receptor potential vanilloid 1… CONTINUE READING
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