ReviewNeuroscience letters2008
Activation of JNK pathway in persistent pain.
Review in Neuroscience letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 143 citations in OpenAlex.
- Botulinum toxin type A attenuates trigeminal neuralgia-like pain by suppressing CGRP release and modulating NaV1.7-associated signaling.The journal of headache and pain · 2026Article
- Cancer-induced nerve injury unveils a sympathetic-to-sensory nerve axis in a mouse model of head and neck squamous cell carcinoma.Science translational medicine · 2026Article
- Dual CCR2/CCR5 Antagonism with Cenicriviroc Alleviates Nerve Injury-Induced Hypersensitivity and Prevents Morphine Tolerancevia Modulation of Neuroimmune Signaling.Cellular and molecular neurobiology · 2026Article
- The Small Molecule Compound Eupalinolide B Ameliorates Depressive Behaviors and Neuropathic Pain in Mice With Spared Nerve Injury: Integrating Network Pharmacology, Molecular Docking, Bioinformatics, Molecular Dynamics Simulation and Experimental Verification.CNS neuroscience & therapeutics · 2026Article
- Cytokine Dynamics in Bortezomib-Induced Peripheral Neuropathy: Challenges in Translating Preclinical Findings to Humans.Journal of the peripheral nervous system : JPNS · 2026Observational
- Epidermal growth factor receptor signaling modulates postoperative pain and inflammatory responses.Frontiers in immunology · 2026Review
- Article
- Molecular Mechanisms Underlying Burn-Injury Induced Pain: From Inflammation to Epigenetics.Military medicine · 2025Review
- Neural Correlates of Peripheral Inflammation in Major Depressive Disorder and Their Transcriptomic Architecture, Neurochemical Basis, and Behavioral Relevance.Human brain mapping · 2025Article
- Closed-Loop Spinal Cord Stimulation in Chronic Pain Management: Mechanisms, Clinical Evidence, and Emerging Perspectives.Biomedicines · 2025Review
- Neuroinflammatory Pathways Associated with Chronic Post-Thoracotomy Pain: A Review of Current Literature.Molecular neurobiology · 2025Review
- Battling pain from osteoarthritis: causing novel cell death.Acta biochimica et biophysica Sinica · 2024Review
- Apocynin Prevents Cigarette Smoke-Induced Anxiety-Like Behavior and Preserves Microglial Profiles in Male Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- Chronic pain as an emergent property of a complex system and the potential roles of psychedelic therapies.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
- The Role of miRNAs in Neuropathic Pain.Biomedicines · 2023Review
- Acupuncture Relieves Cervical Spondylosis Radiculopathy by Regulating Spinal Microglia Activation Through MAPK Signaling Pathway in Rats.Journal of pain research · 2023Article
- The Spatial Extent of Pain Is Associated with Pain Intensity, Catastrophizing and Some Measures of Central Sensitization in People with Frozen Shoulder.Journal of clinical medicine · 2021Article
- Sex and dose-dependent antinociceptive effects of the JNK (c-Jun N-terminal kinase) inhibitor SU 3327 are mediated by CBBrain research bulletin · 2021Article
- Specialized Pro-Resolving Lipid Mediators: The Future of Chronic Pain Therapy?International journal of molecular sciences · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The c-Jun N-terminal kinase (JNK) is a stress-activated member of MAP kinase family. JNK activation has been strongly implicated in inflammatory responses, neurodegeneration, and apoptosis. Recent evidence shows that JNK pathway is also transiently activated in primary sensory neurons after tissue or nerve injury, which is required for the development of hyperalgesia and allodynia. In particular, JNK is persistently activated in astrocytes of the spinal cord after nerve injury, and this activation can maintain central sensitization and mechanical allodynia. In this mini-review, we will provide evidence for the involvement of JNK pathway in regulating persistent pain sensitization. We will also discuss possible upstream signaling mechanisms that cause JNK activation and downstream signaling mechanisms by which JNK modulates pain sensitivity. Thus, targeting JNK pathway might be a useful strategy to treat both neurodegeneration and chronic pain.
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Identifiers
What OpenQuestion holds
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 OpenQuestion graph.