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Knockdown of programmed cell death factor 4 restores erectile function by attenuating apoptosis in rats with bilateral cavernous nerve crush injury.

Yunlong GeTian XiaZejia FengYuhang XiDaoyuan HuYude HongBowen TangJianjie WuJialiang ChenHengjun Xiao
Published in: Andrology (2024)
Elevated programmed cell death factor 4 expression may be an important pathogenetic mechanism for erectile dysfunction after bilateral cavernous nerve crush, and the knockdown of programmed cell death factor 4 enhanced erectile function in 18-month-old rats after cavernous nerve damage. The potential mechanism may be the stimulation of the PI3K/AKT pathway to attenuate the cavernous apoptosis level.
Keyphrases
  • oxidative stress
  • endoplasmic reticulum stress
  • peripheral nerve
  • cell cycle arrest
  • cell death
  • poor prognosis
  • case report
  • optic nerve
  • climate change
  • binding protein