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Extracellular signal-regulated kinases (ERK) 1 and 2 as a key molecule in pain research

Masahiro Kondo1, Ikuko Shibuta2

  • 1Department of Legal Medicine, Nihon University School of Dentistry.

Journal of Oral Science
|April 1, 2020
PubMed

Insights

Extracellular signal-regulated kinases (ERK) 1 and 2 are crucial in pain signaling pathways. Inhibiting ERK shows promise for treating pathological pain, highlighting its potential as a novel therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Pain is classified into nociceptive, inflammatory, and neuropathic types.
  • Understanding pain's molecular mechanisms is key for developing effective pain relief therapies.
  • Extracellular signal-regulated kinases (ERK) 1 and 2, part of the mitogen-activated protein kinase superfamily, were identified 20 years ago.

Purpose of the Study:

  • To review recent advances in understanding the regulation of ERK in pain research.
  • To highlight the role of ERK in pain signaling pathways.
  • To explore the potential of ERK as a novel therapeutic target for pain management.

Main Methods:

  • Review of existing literature on ERK activation in pain signaling.
  • Analysis of studies investigating the effects of ERK inhibition on pathological pain.
  • Examination of ERK expression patterns in various neuronal and glial cells following peripheral nerve injury.

Main Results:

  • Peripheral nerve injury induces ERK activation in glial cells, sensory neurons, and second-order neurons at distinct time points.
  • Inhibition of ERK signaling effectively suppresses pathological pain in animal models of peripheral nerve injury.
  • ERK is confirmed as a significant molecule involved in pain signaling.

Conclusions:

  • ERK plays a critical role in the molecular mechanisms of pain signaling.
  • ERK represents a promising novel target for the development of new pain relief therapies.
  • Further research into ERK regulation is essential for advancing pain treatment strategies.
Keywords:
ERK phosphorylationinflammationnociceptionpainperipheral nerve injurytissue damage

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