Mfn2 downregulation in excitotoxicity causes mitochondrial dysfunction and delayed neuronal death.

@article{MartorellRiera2014Mfn2DI,
  title={Mfn2 downregulation in excitotoxicity causes mitochondrial dysfunction and delayed neuronal death.},
  author={Alejandro Martorell-Riera and Marc Segarra-Mondejar and Juan Pablo Mu{\~n}oz and Vanessa Ginet and Jordi Olloquequi and Je{\'u}s P{\'e}rez-Clausell and Manuel Palac{\'i}n and Manuel Reina and Julien P. Puyal and Antonio Zorzano and Francesc X Soriano},
  journal={The EMBO journal},
  year={2014},
  volume={33 20},
  pages={2388-407}
}
Mitochondrial fusion and fission is a dynamic process critical for the maintenance of mitochondrial function and cell viability. During excitotoxicity neuronal mitochondria are fragmented, but the mechanism underlying this process is poorly understood. Here, we show that Mfn2 is the only member of the mitochondrial fusion/fission machinery whose expression is reduced in in vitro and in vivo models of excitotoxicity. Whereas in cortical primary cultures, Drp1 recruitment to mitochondria plays a… CONTINUE READING
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