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Microglia-derived neuroinflammatory pathways in neuropathic pain
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DOI：10.3344/kjp.25166.png)
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Abstract
En 中文
Neuropathic pain (NP) is a chronic pain condition resulting from damage or disease in the nervous system. It is characterized by hyperalgesia, spontaneous pain, and mechanical allodynia. Due to limited treatment options, NP significantly impairs the quality of life of affected individuals. Recent research has highlighted the critical role of microglia in the initiation and maintenance of NP, however, the underlying mechanisms remain incompletely understood. Existing evidence suggests that signaling pathways, including NF-kappa B, PI3K/Akt/mTOR, p38MAPK, JAK2/STAT3, and Nrf2/HO-1, contribute to microglial activation and the modulation of NP. This review explores the key activation molecules in these pathways, the microglial phenotype, and associated inflammatory processes. Additionally, the authors summarize the latest literature and application prospects of certain drugs/compounds/ non-invasive treatments, aiming to provide a theoretical basis for the development of novel microglia-targeted therapies.
Keywords:
Microglia
Neuralgia
Neuroinflammatory Diseases
NF-E2-Related Factor 2
NF-kappa B
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
TOR Serine-Threonine Kinases
Journal
K
IF:
3.1
Papers:
484
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1.3K
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Cited Papers