p38 mitogen-activated protein kinase and pain
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Updated: Dec 20, 2025

Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats
Published on: January 21, 2020
Lijia Mai1, Xiao Zhu2, Fang Huang3
1Department of Anesthesiology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510080, China; Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510080, China.
Abstract:
Inflammatory and neuropathic pain is initiated by tissue inflammation and nerve injury, respectively. Both are characterized by increased activity in the peripheral and central nervous system, where multiple inflammatory cytokines and other active molecules activate different signaling pathways that involve in the development and/or maintenance of pain. P38 mitogen-activated protein kinase (MAPK) is one member of the MAPK family, which is activated in neurons and glia and contributes importantly to inflammatory and neuropathic pain. The aim of this review is to summarize the latest advances made about the implication of p38 MAPK signaling cascade in pain. It can deepen our understanding of the molecular mechanisms of pain and may help to offer new targets for pain treatment.
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