Silencing of fas, fas-associated via death domain, or caspase 3 differentially affects lung inflammation, apoptosis, and development of trauma-induced septic acute lung injury.

@article{Messer2013SilencingOF,
  title={Silencing of fas, fas-associated via death domain, or caspase 3 differentially affects lung inflammation, apoptosis, and development of trauma-induced septic acute lung injury.},
  author={Mirko Philipp Messer and Philipp Kellermann and Sascha J{\"o}rn Weber and Christoph Hohmann and Stephanie Denk and Bettina Klohs and Anke Schultze and Sonja T Braum{\"u}ller and Markus S Huber-Lang and Mario Perl},
  journal={Shock},
  year={2013},
  volume={39 1},
  pages={
          19-27
        }
}
Activation of Fas signaling is a potentially important pathophysiological mechanism in the development of septic acute lung injury (ALI). However, so far the optimal targets within this signaling cascade remain elusive. Thus, we tested the hypothesis that in vivo gene silencing of Fas, Fas-associated via death domain (FADD), or caspase 3 by intratracheal administration of small interfering RNA would ameliorate ALI in a clinically relevant double-hit mouse model of trauma induced septic lung… CONTINUE READING
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