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Molecular Mechanism and Pathophysiology of Pain

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (25 November 2024) | Viewed by 1698

Special Issue Editor


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Guest Editor
Miami Project to Cure Paralysis, Miller School of Medicine University of Miami, 1095 NW 14th Terrace, Miami, FL 33136, USA
Interests: chronic pain; molecular signaling; cell therapy; gene therapy; stem cells; spinal cord injury; peripheral nerve injury

Special Issue Information

Dear Colleagues,

This Special Issue, entitled "Molecular Mechanisms and Pathophysiology of Pain," delves into the intricate biological processes governing the perception, transmission, and modulation of pain signals within the nervous system. The aim of this Special Issue is to contribute to the clarification of the interplay of various molecular components, including neurotransmitters, receptors, ion channels, and signaling molecules, within the peripheral nerves, spinal cord, and brain regions involved in pain processing. Dysregulation of these molecular mechanisms can lead to chronic pain conditions, including neuropathic pain and inflammatory pain syndromes. Additionally, epigenetic modifications, including DNA methylation and histone modifications, play a crucial role in modulating gene expression and shaping the molecular landscape underlying pain perception. Understanding these mechanisms is essential for developing targeted therapies aimed at alleviating pain and improving the quality of life for individuals affected by acute and chronic pain conditions. By unraveling the complexities of pain biology and identifying novel therapeutic targets, research in this field holds promise for advancing pain management strategies and personalized treatment approaches tailored to the individual patient’s unique molecular profiles. We warmly welcome submissions, including original papers and reviews, focused on (1) novel mechanisms of pain signaling in the peripheral and central nervous systems; (2) mechanisms of chronic pain development; (3) molecular and epigenetic changes involved in pathological pain; (4) novel pain models; and (5) translational studies with therapeutical approaches.

Dr. Stanislava Jergová
Guest Editor

Manuscript Submission Information

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Keywords

  • acute pain mechanism
  • chronic pain mechanisms
  • pain receptors and neurotransmitter
  • epigenetic changes in pain
  • pain therapy
  • gene therapy in pain
  • cell therapy in pain
  • pain models
 
 
 
 
 

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Published Papers (1 paper)

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Research

16 pages, 1922 KiB  
Article
Gene Expression Correlates with Disability and Pain Intensity in Patients with Chronic Low Back Pain and Modic Changes in a Sex-Specific Manner
by Maria Dehli Vigeland, Siri Tennebø Flåm, Magnus Dehli Vigeland, Manuela Zucknick, Monica Wigemyr, Lars Christian Haugli Bråten, Elisabeth Gjefsen, John-Anker Zwart, Kjersti Storheim, Linda Margareth Pedersen, Benedicte Alexandra Lie and the AIM Study Group
Int. J. Mol. Sci. 2025, 26(2), 800; https://doi.org/10.3390/ijms26020800 - 18 Jan 2025
Viewed by 1182
Abstract
Chronic low back pain (cLBP) lacks clear physiological explanations, and the treatment options are of limited effect. We aimed to elucidate the underlying biology of cLBP in a subgroup of patients with Modic changes type I (suggestive of inflammatory vertebral bone marrow lesions) [...] Read more.
Chronic low back pain (cLBP) lacks clear physiological explanations, and the treatment options are of limited effect. We aimed to elucidate the underlying biology of cLBP in a subgroup of patients with Modic changes type I (suggestive of inflammatory vertebral bone marrow lesions) by correlating gene expression in blood with patient-reported outcomes on disability and pain intensity and explore sex differences. Patients were included from the placebo group of a clinical study on patients with cLBP and Modic changes. Blood was collected at the time of inclusion, after three months, and after one year, and gene expression was measured at all time points by high-throughput RNA sequencing. The patients reported disability using the Roland–Morris Disability Questionnaire, and pain intensity was assessed as a mean of three scores on a 0–10 numeric rating scale: current LBP, worst LBP within the last two weeks, and mean LBP within the last two weeks. The gene expression profiles were then correlated to the reported outcomes. Changes in gene expression over time correlated significantly with changes in both disability and pain. The findings showed distinct patterns in men and women, with negligible overlap in correlated genes between the sexes. The genes involved were enriched in immunological pathways, particularly T cell receptor complex and immune responses related to neutrophils. Several of the genes harbour polymorphisms that previously have been found to be associated with chronic pain. Taken together, our results indicate gender differences in the underlying biology of disability and pain intensity in patients with low back pain. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathophysiology of Pain)
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