The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Emerging targets in neuroinflammation-driven chronic pain
Open accessAbstract
Current analgesics predominately modulate pain transduction and transmission in neurons and have limited success in controlling disease progression. Accumulating evidence suggests that neuroinflammation, which is characterized by infiltration of immune cells, activation of glial cells and production of inflammatory mediators in the peripheral and central nervous system, has an important role in the induction and maintenance of chronic pain. This Review focuses on emerging targets — such as chemokines, proteases and the WNT pathway — that promote spinal cord neuroinflammation and chronic pain. It also highlights the anti-inflammatory and pro-resolution lipid mediators that act on immune cells, glial cells and neurons to resolve neuroinflammation, synaptic plasticity and pain. Targeting excessive neuroinflammation could offer new therapeutic opportunities for chronic pain and related neurological and psychiatric disorders.
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Cites
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Self-citation
Cited by
Neuroinflammation and Central Sensitization in Chronic and Widespread Pain
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Self-citationPain regulation by non-neuronal cells and inflammation
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Therapeutic options for targeting inflammatory osteoarthritis pain
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Mechanism-based treatment for chemotherapy-induced peripheral neuropathic pain
Sisignano, M., Baron, R., Scholich, K., & Geisslinger, G. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.211 · Cited by 344
Metadata
- Authors
- Ji, R.-R., Xu, Z.-Z., & Gao, Y.-J.
- Venue
- Nature Reviews Drug Discovery
- Published
- 2014-06-20
- Volume
- 13
- Issue
- 7
- Pages
- 533-548
- ISSN
- 1474-1776 (ISSN-L)
- 1474-1784
- OpenAlex
- W2046296795
- Cited by
- 1,101
- References
- 23
- FWCI
- 8.01
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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