ReviewBrain research reviews2009
MAP kinase and pain.
Review in Brain research reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 524 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
524 citing papers in PubMed, 973 citations in OpenAlex.
- Effects of Acute Fish Oil Supplementation on Muscle Function and Soreness After Eccentric Contraction-Induced Muscle Damage.Nutrients · 2025Trial
- Peripheral nerve injury alters metabolic function and neuronal excitability through the Lin28/let-7 pathway.Science advances · 2026Article
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Drug-specific effects of anxiety on high-dose oxycodone: age as a modifier for oxycodone response.Behavioural pharmacology · 2026Article
- Development of G Protein-Coupled Receptor 183 Benzimidazole Antagonists Utilizing a Core-Hopping Approach.Molecules (Basel, Switzerland) · 2026Article
- TMJ hyperextension is associated with sustained nociception and dysfunction of pain modulation pathways in female rats.Cranio : the journal of craniomandibular practice · 2026Article
- Catecholamine-mediated release of miR-133a-3p from adipocytes regulates the onset of chronic primary pain.The Journal of clinical investigation · 2026Article
- 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
- Review
- Dual CCR2/CCR5 Antagonism with Cenicriviroc Alleviates Nerve Injury-Induced Hypersensitivity and Prevents Morphine Tolerancevia Modulation of Neuroimmune Signaling.Cellular and molecular neurobiology · 2026Article
- Intense pulsed light rejuvenates UVB-induced photoaging in human keratinocytes and guinea pig skin by inhibition of ERK-AP-1-MMP pathway.Scientific reports · 2026Article
- Article
- From Amputation to Persistent Pain: A Review of Molecular and Cellular Processes in Phantom Limb Pain.International journal of molecular sciences · 2026Review
- Modulation of Nociceptive Ion Channels by Protease-Activated Receptor-2 in Inflammatory Pain: Molecular Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Nicorandil ameliorates neuropathic and inflammatory pain via TNF-α, IL6/MAPKScientific reports · 2026Article
- Peripheral Immune and Metabolic Dysregulation in Migraine, Ménière's Disease, and Vestibular Migraine: A Single-Cell Atlas Study.Human mutation · 2026Article
- Neuroimmune regulation of visceral pain: roles of microglia, purinergic signaling, and neuroinflammation.Frontiers in immunology · 2026Review
- An Integrative Framework Identifies Cooperative Targeting of Host Pathways by Tick Salivary miRNAs.Computational and structural biotechnology journal · 2026Article
- Article
- Inhibition of P2X7 receptor in satellite glial cells contributes to electroacupuncture's analgesia in rats with CFA-induced inflammatory pain.Chinese medicine · 2025Article
464 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitogen-activated protein kinases (MAPKs) are important for intracellular signal transduction and play critical roles in regulating neural plasticity and inflammatory responses. The MAPK family consists of three major members: extracellular signal-regulated kinases (ERK), p38, and c-Jun N-terminal kinase (JNK), which represent three separate signaling pathways. Accumulating evidence shows that all three MAPK pathways contribute to pain sensitization after tissue and nerve injury via distinct molecular and cellular mechanisms. Activation (phosphorylation) of MAPKs under different persistent pain conditions results in the induction and maintenance of pain hypersensitivity via non-transcriptional and transcriptional regulation. In particular, ERK activation in spinal cord dorsal horn neurons by nociceptive activity, via multiple neurotransmitter receptors, and using different second messenger pathways plays a critical role in central sensitization by regulating the activity of glutamate receptors and potassium channels and inducing gene transcription. ERK activation in amygdala neurons is also required for inflammatory pain sensitization. After nerve injury, ERK, p38, and JNK are differentially activated in spinal glial cells (microglia vs astrocytes), leading to the synthesis of proinflammatory/pronociceptive mediators, thereby enhancing and prolonging pain. Inhibition of all three MAPK pathways has been shown to attenuate inflammatory and neuropathic pain in different animal models. Development of specific inhibitors for MAPK pathways to target neurons and glial cells may lead to new therapies for pain management. Although it is well documented that MAPK pathways can increase pain sensitivity via peripheral mechanisms, this review will focus on central mechanisms of MAPKs, especially ERK.
Indexed as
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.