ReviewFrontiers in pharmacology2023
The role of neuroinflammation in the transition of acute to chronic pain and the opioid-induced hyperalgesia and tolerance.
Review in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.
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
41 citing papers in PubMed, 3 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Sexually Dimorphic Neuroimmune Pathways in Chronic Pain: A Comprehensive Systematic Review of Cellular and Molecular Mechanisms.Biomolecules · 2026Pooled it
- Opioid conversion in adults with cancer: MASCC-ASCO-AAHPM-HPNA-NICSO guideline.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025Guideline
- Extended Treatment with Micron-Size Oral Palmitoylethanolamide (PEA) in Chronic Pain: A Systematic Review and Meta-Analysis.Nutrients · 2024Pooled it
- Early repetitive transcranial magnetic stimulation for preventing chronic postoperative pain in older adults: a randomized clinical sub-study.BMC medicine · 2026Trial
- Memantine treatment improves opioid-induced hyperalgesia symptoms: randomize clinical trial.Scientific reports · 2025Trial
- Integrated analysis of single-cell and transcriptome data reveals temporal dynamics of microglial phagocytic reprogramming in neuropathic pain progression.Scientific reports · 2026Article
- Antinociceptive Effects of Free and β-Cyclodextrin-Associated α-Phellandrene in CFA-Induced Inflammatory Pain.Biomedicines · 2026Article
- Can Chronic Pain Accelerate Chronic Kidney Disease? Is Pain a Disease Modifier Rather than a Symptom?Life (Basel, Switzerland) · 2026Article
- Discovery of a peripherally restricted αCell reports. Medicine · 2026Article
- Neuromodulation strategies in postburn care for pain rehabilitation and scar remodelling.Communications medicine · 2026Review
- Targeting Neuroinflammation and Peripheral Nerve Dysfunction in Refractory Postherpetic Neuralgia: A Multimodal Injection Case Series.The American journal of case reports · 2026Article
- Kratom (Molecules (Basel, Switzerland) · 2026Article
- Repurposed Systemic Pharmacologic Agents in Chronic Pain: Emerging Mechanistic and Clinical Insights.Journal of clinical medicine · 2026Review
- Article
- Emerging Nonpharmacologic Analgesic Technologies in Anesthesia: Mechanisms, Evidence, and Future Directions for Pharmacologic Alternatives.Biomedicines · 2026Review
- Astrocytes in Parkinson's Disease: From Guardians to Accomplices.Clinical interventions in aging · 2026Review
- Transcriptional signatures of aberrant brain functional network topology in chronic low back pain with lumbar disc herniation.Frontiers in molecular neuroscience · 2026Article
- Inflammatory Cytokine-Mediated Interactions Between Pain and Insomnia: Mechanisms and Therapeutic Implications.Journal of pain research · 2026Review
- Review
- Metabolite-neuro-immune relay in chronic pain: spatial-temporal lactate, succinate and itaconate signalling as drivers of glial reprogramming and neuronal sensitisation.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current evidence suggests that activation of glial and immune cells leads to increased production of proinflammatory mediators, creating a neuroinflammatory state. Neuroinflammation has been proven to be a fundamental mechanism in the genesis of acute pain and its transition to neuropathic and chronic pain. A noxious event that stimulates peripheral afferent nerve fibers may also activate pronociceptive receptors situated at the dorsal root ganglion and dorsal horn of the spinal cord, as well as peripheral glial cells, setting off the so-called peripheral sensitization and spreading neuroinflammation to the brain. Once activated, microglia produce cytokines, chemokines, and neuropeptides that can increase the sensitivity and firing properties of second-order neurons, upregulating the signaling of nociceptive information to the cerebral cortex. This process, known as central sensitization, is crucial for chronification of acute pain. Immune-neuronal interactions are also implicated in the lesser-known complex regulatory relationship between pain and opioids. Current evidence suggests that activated immune and glial cells can alter neuronal function, induce, and maintain pathological pain, and disrupt the analgesic effects of opioid drugs by contributing to the development of tolerance and dependence, even causing paradoxical hyperalgesia. Such alterations may occur when the neuronal environment is impacted by trauma, inflammation, and immune-derived molecules, or when opioids induce proinflammatory glial activation. Hence, understanding these intricate interactions may help in managing pain signaling and opioid efficacy beyond the classical pharmacological approach.
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