Corrigendum: Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy

@article{Bierhaus2012CorrigendumMM,
  title={Corrigendum: Methylglyoxal modification of Nav1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy},
  author={Angelika Bierhaus and Thomas Fleming and Stoyan Stoyanov and Andreas Leffler and Alexandru Babes and Cristian Neacsu and Susanne K. Sauer and Mirjam Eberhardt and Martina Schnoelzer and Felix Lasischka and Winfried L Neuhuber and Tatjana I Kichko and Ilze Konrade and Ralf Elvert and Walter Mier and Valdis Pīrāgs and Ivan Kre{\vs}imir Luki{\'c} and Michael Morcos and Thomas Dehmer and Naila Rabbani and Paul J. Thornalley and Diane Edelstein and Carla Nau and Josephine M Forbes and Per M. Humpert and Markus Schwaninger and Dan Ziegler and David M. Stern and Mark Emmanuel Cooper and Uwe Haberkorn and Michael Brownlee and Peter W Reeh and Peter P Nawroth},
  journal={Nature Medicine},
  year={2012},
  volume={18},
  pages={926-933}
}
This study establishes a mechanism for metabolic hyperalgesia based on the glycolytic metabolite methylglyoxal. We found that concentrations of plasma methylglyoxal above 600 nM discriminate between diabetes-affected individuals with pain and those without pain. Methylglyoxal depolarizes sensory neurons and induces post-translational modifications of the voltage-gated sodium channel Nav1.8, which are associated with increased electrical excitability and facilitated firing of nociceptive neurons… CONTINUE READING