Evidence map›Paper›PMID 20880510›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2010

Targeting astrocyte signaling for chronic pain.

Yong-Jing Gao, Ru-Rong Ji

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed, 4 pooled it
14.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

229 citing papers in PubMed, 4 syntheses or guidelines pooled it, 414 citations in OpenAlex.

  1. Pooled it
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  5. Glial cells in neuropathic pain.Physiological reviews · 2026
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  10. iRhom2 deletion protects against diabetic neuropathy by suppressing neuroinflammation.The Journal of pharmacology and experimental therapeutics · 2026
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169 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Yong-Jing GaoDepartment of Anesthesiology, Sensory Plasticity Laboratory, Pain Research Center, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. yjing@zeus.bwh.harvard.edu
Ru-Rong Ji
Brigham and Women's Hospital · USHarvard University · US

Funding

Neuronal and glial interactions of neuropathic painR01DE017794 · NIDCR · DUKE UNIVERSITY · PI BUCHHEIT, THOMAS · 2006 to 2021
$6.6M
Resolvins, protectins, and chronic pain resolution.R01NS067686 · NINDS · DUKE UNIVERSITY · PI JI, RU-RONG, SERHAN, CHARLES NICHOLAS · 2009 to 2013
$2.8M
Astroglial mechanisms for inflammatory painR01NS054932 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI JI, RU-RONG · 2007 to 2010
$1.4M
NIDCR NIH HHS R01 DE017794NIDCR NIH HHS R01 DE17794NINDS NIH HHS R01 NS054932NINDS NIH HHS R01 NS067686NINDS NIH HHS R01 NS54932NINDS NIH HHS R01 NS67686
6 · The paper itself

Abstract

Clinical management of chronic pain after nerve injury (neuropathic pain) and tumor invasion (cancer pain) is a real challenge due to our limited understanding of the cellular mechanisms that initiate and maintain chronic pain. It has been increasingly recognized that glial cells, such as microglia and astrocytes in the CNS play an important role in the development and maintenance of chronic pain. Notably, astrocytes make very close contacts with synapses and astrocyte reaction after nerve injury, arthritis, and tumor growth is more persistent than microglial reaction, and displays a better correlation with chronic pain behaviors. Accumulating evidence indicates that activated astrocytes can release pro-inflammatory cytokines (e.g., interleukin [IL]-1β) and chemokines (e.g., monocyte chemoattractant protein-1 [MCP-1]/also called CCL2) in the spinal cord to enhance and prolong persistent pain states. IL-1β can powerfully modulate synaptic transmission in the spinal cord by enhancing excitatory synaptic transmission and suppressing inhibitory synaptic transmission. IL-1β activation (cleavage) in the spinal cord after nerve injury requires the matrix metalloprotease-2. In particular, nerve injury and inflammation activate the c-Jun N-terminal kinase in spinal astrocytes, leading to a substantial increase in the expression and release of MCP-1. The MCP-1 increases pain sensitivity via direct activation of NMDA receptors in dorsal horn neurons. Pharmacological inhibition of the IL-1β, c-Jun N-terminal kinase, MCP-1, or matrix metalloprotease-2 signaling via spinal administration has been shown to attenuate inflammatory, neuropathic, or cancer pain. Therefore, interventions in specific signaling pathways in astrocytes may offer new approaches for the management of chronic pain.

Indexed as

Pain ManagementAnimalsAstrocytesChronic DiseaseCytokinesHumansInflammationMAP Kinase Signaling SystemPainCytokines

Identifiers

PMID20880510
PMCPMC2950097
OpenAlexW2016936987

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.