Chronic Pain and Oxidative Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1236

Special Issue Editor

Grup de Neurofarmacologia Molecular, Institut de Recerca Sant Pau, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain
Interests: analgesia; anxiety; depression; cannabinoids; carbon monoxide; heme oxygenase 1; hydrogen sulfide; molecular hydrogen; nitric oxide; Nrf2 transcription factor; oxidative stress; pain; opioids
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Special Issue Information

Dear Colleagues,

Chronic pain affects a high percentage of the population, making it a serious global health problem. Current therapies are ineffective and have significant side effects, negatively affecting the patients' quality of life.  Research into new treatments capable of effectively relieving chronic pain with few adverse effects constitutes a major challenge.

Oxidative stress and inflammation are two of the main mechanisms involved in the development of chronic pain, both of which can lead to mitochondrial dysfunction. Moreover, oxidative stress can activate redox-sensitive inflammatory mediators, causing uncontrolled inflammatory reactions that heighten pain sensitivity. Further studies are needed to clarify the molecular mechanisms involved in this process to identify new compounds as potential therapeutic targets for chronic pain.

The antioxidant system activated by the Nrf2 transcription factor serves as an endogenous defense mechanism against oxidative stress by reducing ROS levels, inflammatory responses, and mitochondrial impairment. The analgesic properties of several Nrf2-inducing compounds, such as sulforaphane and oltipraz, have been identified in various preclinical models of inflammatory and neuropathic pain. However, there is a wide range of antioxidant compounds whose analgesic properties and mechanisms of action have yet to be identified. This Special Issue titled "Chronic Pain and Oxidative Stress" aims to compile original research articles that evaluate the analgesic properties of novel compounds and their effects on oxidative stress, proinflammatory signals, and plasticity changes caused by inflammation, nerve injury, chemotherapeutic agents, and/or metabolic disorders. We believe this Special Issue will advance research into new, effective, and safe strategies for treating chronic pain that can be used in clinical practice.

As the Guest Editor, I invite you to contribute to this Special Issue.

I look forward to your contributions.

Dr. Olga Pol
Guest Editor

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Keywords

  • analgesia
  • antioxidants
  • chemotherapy
  • heme oxygenase 1
  • neuropathy
  • nociception
  • Nrf2 transcription factor
  • oxidative stress
  • pain

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Published Papers (1 paper)

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Review

44 pages, 9564 KB  
Review
Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk
by Bojan Stojanovic, Ivana Milivojcevic Bevc, Milica Dimitrijevic Stojanovic, Bojana S. Stojanovic, Tatjana Lazarevic, Marko Spasic, Marko Petrovic, Ivana Stefanovic, Marina Markovic, Jelena Nesic, Danijela Jovanovic, Miodrag Peulic, Ana Azanjac Arsic, Ana Lukovic, Nikola Mirkovic, Stevan Eric and Nenad Zornic
Antioxidants 2025, 14(10), 1166; https://doi.org/10.3390/antiox14101166 - 25 Sep 2025
Viewed by 986
Abstract
Neuropathic pain is a chronic condition driven by intertwined mechanisms of oxidative stress, inflammation, and cellular senescence. Nerve injury and metabolic stress elevate reactive oxygen and nitrogen species, disrupt mitochondrial function, and activate the DNA-damage response, which stabilizes p53 and induces p16/p21-mediated cell-cycle [...] Read more.
Neuropathic pain is a chronic condition driven by intertwined mechanisms of oxidative stress, inflammation, and cellular senescence. Nerve injury and metabolic stress elevate reactive oxygen and nitrogen species, disrupt mitochondrial function, and activate the DNA-damage response, which stabilizes p53 and induces p16/p21-mediated cell-cycle arrest. These events promote a senescence-associated secretory phenotype (SASP) rich in cytokines, chemokines, and prostanoids that amplify neuroimmune signaling. In the spinal dorsal horn and dorsal root ganglia, microglia and astroglia respond to redox imbalance and danger cues by engaging NF-κB and MAPK pathways, increasing COX-2–dependent prostaglandin synthesis, and releasing mediators such as IL-1β and BDNF that enhance synaptic transmission and reduce inhibitory tone through KCC2 dysfunction. At the periphery, persistent immune-glial cross-talk lowers activation thresholds of nociceptors and sustains ectopic firing, while impaired autophagy and mitophagy further exacerbate mitochondrial dysfunction and ROS production. Collectively, these processes establish a feed-forward loop in which redox imbalance triggers senescence programs and SASP, SASP perpetuates neuroinflammation, and neuroinflammation maintains central sensitization—thereby consolidating a self-sustaining redox–senescence–inflammatory circuit underlying neuropathic pain chronicity. Full article
(This article belongs to the Special Issue Chronic Pain and Oxidative Stress)
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