ReviewAntioxidants (Basel, Switzerland)2025
Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed.
- Effects of Kalanchoe pinnata, exercise, and stimulation on neuroinflammation, redox homeostasis, and neuropathic pain in a Wistar-rat model.World journal of experimental medicine · 2026Article
- Relationships between dietary antioxidant capacity, systemic redox balance, and neuropathic pain after spinal cord injury.Spinal cord · 2026Article
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- 7-Hydroxyflavone mitigates partial sciatic nerve ligation-induced neuropathic pain via modulation of oxidative and inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- Temporal multi-omic exploration of the ventral tegmental area in chronic pain and passive coping behaviors.iScience · 2026Article
- Review
- Repurposed Systemic Pharmacologic Agents in Chronic Pain: Emerging Mechanistic and Clinical Insights.Journal of clinical medicine · 2026Review
- Neuroimaging-Guided Insights into the Molecular and Network Mechanisms of Chronic Pain and Neuromodulation.International journal of molecular sciences · 2026Review
- Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.Molecular and cellular biology · 2026Article
- Astrocytes in Neuropathic Pain: Mechanistic and Global Insights.Pain research & management · 2026Review
- A Surface-Engineered Cerium Oxide Nanozyme Functionalized with L-Theanine for Redox and Inflammatory Modulation in Neuropathic Pain.International journal of nanomedicine · 2026Article
- Analgesic and Local Anesthetic Effects of a Clove-Derived Injectable Formulation via Modulation of Oxidative Stress and Nociceptive Signaling.Pain research & management · 2026Article
- Re-Analysis of Public Transcriptomes Identifies a Candidate Histone-Cluster Signal in Eutopic Endometrium: A Hypothesis-Generating Link to Chronic Pelvic Pain.Journal of pain research · 2026Article
- The interaction between oxidative stress and Schwann cells.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Review
- Tuina Analgesia Is Associated With the Modulation of the NCOA4-Mediated Ferroautophagy-Ferroptosis Pathway in SNL-Induced Neuropathic Pain Rats.Pain research & management · 2026Article
- Myofascial pain in older adults: a geroscience-informed framework integrating precision geriatrics and digital therapeutics.Frontiers in aging neuroscience · 2026Review
- The neuro-immuno-metabolic axis of exercise: a unified mechanistic framework for exercise-induced cognitive enhancement and psychological resilience.Frontiers in psychology · 2026Review
- Nrf2 as a Molecular Guardian of Redox Balance and Barrier Integrity in IBD.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
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 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.