Abstract
Chronic pain, often defined as any pain lasting more than 3 months, is poorly managed because of its multifaceted and complex mechanisms. Calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinase that plays a fundamental role in synaptic plasticity, learning, and memory. Recent emerging evidence demonstrates increased expression and activity of CaMKII in the spinal cord and dorsal root ganglia of various chronic pain models. Moreover, our previous studies also find that inhibiting CaMKII could attenuate inflammatory pain and neuropathic pain. In this review, we provide evidence for the involvement of CaMKII in the initiation and development of chronic pain, including neuropathic pain, bone cancer pain, and inflammatory pain. Novel CaMKII inhibitors with potent inhibitory effect and high specificity may be alternative therapeutic strategies for the management of chronic pain in the future.
Footnotes
- Received May 24, 2017.
- Accepted August 28, 2017.
↵1 Y.-Q.Z. and D.-Q.L. contributed equally to this work.
This work was supported by grants from National Natural Science Foundation of P.R. China 81400917, 81371250, 81571053, and 81771196.
- Copyright © 2017 by The American Society for Pharmacology and Experimental Therapeutics
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