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Cited by 624

The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.

p38 MAPK, Microglial Signaling, and Neuropathic Pain

Open access
Ji, Ru-Rong, Suter, Marc R·2007·Molecular Pain

Abstract

Accumulating evidence over last several years indicates an important role of microglial cells in the pathogenesis of neuropathic pain. Signal transduction in microglia under chronic pain states has begun to be revealed. We will review the evidence that p38 MAPK is activated in spinal microglia after nerve injury and contributes importantly to neuropathic pain development and maintenance. We will discuss the upstream mechanisms causing p38 activation in spinal microglia after nerve injury. We will also discuss the downstream mechanisms by which p38 produces inflammatory mediators. Taken together, current data suggest that p38 plays a critical role in microglial signaling under neuropathic pain conditions and represents a valuable therapeutic target for neuropathic pain management.

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Crossref · 10.1186/1744-8069-3-33

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Metadata

Authors
Ji, R.-R., & Suter, M. R.
Venue
Molecular Pain
Published
2007-01-01
Volume
3
Pages
33-33
ISSN
1744-8069 (ISSN-L)
OpenAlex
W2135247591
Cited by
624
References
69
FWCI
17.20
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: p38 MAPK, Microglial Signaling, and Neuropathic Pain. https://app.cochat.ai/papers/10.1186/1744-8069-3-33
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Ji, R.-R., & Suter, M. R. (2007). p38 MAPK, Microglial Signaling, and Neuropathic Pain. Molecular Pain. https://doi.org/10.1186/1744-8069-3-33

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.