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Molecular Mechanisms of Chronic Pain

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1551

Special Issue Editors


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Guest Editor
A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, Neulaniementie 2, 70211 Kuopio, Finland
Interests: synaptic transmission; neuronal plasticity; neuron–glia interactions; neuronal networks; purinergic mechanisms; mechanosensitive ion channels; neurotransmitter receptors in health and disease; receptor desensitization; receptor trafficking; modelling of receptor kinetics; mitochondria; reactive oxygen species; molecular and cellular mechanisms of pain and analgesia; migraine; neuroprotection
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Guest Editor
1. Department of Human Genetics, Leiden University Medical Centre, 2333 ZA Leiden, The Netherlands
2. Department of Neurology, Leiden University Medical Centre, 2333 ZA Leiden, The Netherlands
Interests: neurogenetics; neurobiology; translational research; migraine; primary headaches; ataxia; epilepsy; molecular genetics; genome-wide association studies; next-generation sequencing; omics techniques

Special Issue Information

Dear Colleagues,

Chronic pain is defined as persistent pain that lasts beyond the healing time. This disabling condition affects a large portion of the world’s population and can significantly impact their quality of life. Unfortunately, chronic pain treatment is often ineffective, primarily due to the heterogeneous/multifactorial nature of the condition and our limited knowledge of the underlying mechanisms. However, this field is evolving, offering new concepts concerning the functional role of different types of pain and uncovering new molecular players involved in this complex pathological condition. Our deep understanding of the molecular mechanisms of chronic pain is crucial for the development of new, effective treatment options tailored to patients with chronic pain.

In the current Special Issue, entitled ‘Molecular Mechanisms of Chronic Pain’, we aim to address the cellular and molecular mechanisms of chronic pain studied in animal models as well as patients with this disorder.

We invite researchers working in this area to submit original papers as well as review articles primarily focusing on the molecular mechanisms of chronic pain.

Prof. Dr. Rashid Giniatullin
Prof. Dr. Arn M.J.M. van den Maagdenberg
Guest Editors

Manuscript Submission Information

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Keywords

  • chronic pain
  • persistent pain
  • neuroprotection
  • molecular mechanisms
  • animal models
  • new treatment options

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Published Papers (1 paper)

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Research

21 pages, 4498 KiB  
Article
Impact of Interleukin-6 Activation and Arthritis on Epidermal Growth Factor Receptor (EGFR) Activation in Sensory Neurons and the Spinal Cord
by Anutosh Roy, Gisela Segond von Banchet, Fátima Gimeno-Ferrer, Christian König, Annett Eitner, Andrea Ebersberger, Matthias Ebbinghaus, Johannes Leuchtweis and Hans-Georg Schaible
Int. J. Mol. Sci. 2024, 25(13), 7168; https://doi.org/10.3390/ijms25137168 - 28 Jun 2024
Cited by 2 | Viewed by 1273
Abstract
In tumor cells, interleukin-6 (IL-6) signaling can lead to activation of the epidermal growth factor receptor (EGFR), which prolongs Stat3 activation. In the present experiments, we tested the hypothesis that IL-6 signaling activates EGFR signaling in peripheral and spinal nociception and examined whether [...] Read more.
In tumor cells, interleukin-6 (IL-6) signaling can lead to activation of the epidermal growth factor receptor (EGFR), which prolongs Stat3 activation. In the present experiments, we tested the hypothesis that IL-6 signaling activates EGFR signaling in peripheral and spinal nociception and examined whether EGFR localization and activation coincide with pain-related behaviors in arthritis. In vivo in anesthetized rats, spinal application of the EGFR receptor blocker gefitinib reduced the responses of spinal cord neurons to noxious joint stimulation, but only after spinal pretreatment with IL-6 and soluble IL-6 receptor. Using Western blots, we found that IL-6-induced Stat3 activation was reduced by gefitinib in microglial cells of the BV2 cell line, but not in cultured DRG neurons. Immunohistochemistry showed EGFR localization in most DRG neurons from normal rats, but significant downregulation in the acute and most painful arthritis phase. In the spinal cord of mice, EGFR was highly activated mainly in the chronic phase of inflammation, with localization in neurons. These data suggest that spinal IL-6 signaling may activate spinal EGFR signaling. Downregulation of EGFR in DRG neurons in acute arthritis may limit nociception, but pronounced delayed activation of EGFR in the spinal cord may be involved in chronic inflammatory pain. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Chronic Pain)
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