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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Related Experiment Video

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Assessment of Knee Hyperalgesia in Mice using Pressure Application Measurement
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Published on: June 13, 2025

MAP kinase and pain.

Ru-Rong Ji1, Robert W Gereau, Marzia Malcangio

  • 1Pain Research Center, Department of Anesthesiology, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, MRB 604, Boston, MA 02115, USA. rrji@zeus.bwh.harvard.edu

Brain Research Reviews
|January 20, 2009
PubMed
Summary
This summary is machine-generated.

Mitogen-activated protein kinase (MAPK) pathways, including ERK, p38, and JNK, are crucial in pain sensitization. Inhibiting these pathways in animal models shows potential for managing inflammatory and neuropathic pain.

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Published on: February 22, 2019

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Mitogen-activated protein kinases (MAPKs) are key regulators of intracellular signal transduction.
  • MAPKs, including ERK, p38, and JNK, are involved in neural plasticity and inflammatory responses.
  • These pathways are implicated in pain sensitization following tissue and nerve injury.

Purpose of the Study:

  • To review the central mechanisms of MAPK pathways in pain sensitization.
  • To highlight the specific role of extracellular signal-regulated kinases (ERK) in central sensitization.
  • To discuss the potential of MAPK pathway inhibitors for pain management.

Main Methods:

  • Review of existing scientific literature on MAPK signaling in pain.
  • Focus on central mechanisms, particularly in the spinal cord dorsal horn and amygdala.
  • Analysis of transcriptional and non-transcriptional regulation by MAPKs.

Main Results:

  • MAPK pathways (ERK, p38, JNK) contribute to pain hypersensitivity through distinct mechanisms.
  • ERK activation in spinal cord neurons is critical for central sensitization, regulating ion channels and gene transcription.
  • Differential activation of MAPKs in spinal glial cells contributes to inflammatory mediator synthesis.
  • Inhibition of MAPK pathways attenuates pain in animal models of inflammatory and neuropathic pain.

Conclusions:

  • MAPK pathways, especially ERK, play significant roles in central pain mechanisms.
  • Targeting neuronal and glial MAPK pathways offers potential therapeutic strategies for pain management.
  • Further research into specific MAPK inhibitors could lead to novel pain therapies.