Suppression of STIM1 in the early stage after global ischemia attenuates the injury of delayed neuronal death by inhibiting store-operated calcium entry-induced apoptosis in rats.

@article{Zhang2014SuppressionOS,
  title={Suppression of STIM1 in the early stage after global ischemia attenuates the injury of delayed neuronal death by inhibiting store-operated calcium entry-induced apoptosis in rats.},
  author={Ming Zhang and Jinning Song and Yuan Wu and Yong-lin Zhao and Hong-gang Pang and Zhou-Feng Fu and Bin-fei Zhang and Xudong Ma},
  journal={Neuroreport},
  year={2014},
  volume={25 7},
  pages={507-13}
}
Ca²⁺ overload is considered to be the most important ion imbalance in the neuronal injury. Store-operated Ca²⁺ entry has been suggested to be a significant mechanism of excessive Ca²⁺ influx in many cells. The role of store-operated Ca²⁺ entry in neuronal ischemic injury has yet to be elucidated. The aim of this study was to assess the role of store-operated calcium channel (SOCC) proteins involved with calcium overload in the induction of delayed neuronal death after global ischemia in rats. A… CONTINUE READING