Cellular and Molecular Mechanisms of Calcium/Calmodulin-Dependent Protein Kinase II in Chronic Pain.

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.

• Authors: Ya-Qun Zhou, Dai-Qiang Liu, Shu-Ping Chen, Jia Sun, Xue-Rong Zhou, Fang Luo, Yu-Ke Tian, Da-Wei Ye
• Journal: The Journal of pharmacology and experimental therapeutics (J Pharmacol Exp Ther) Vol. 363 Issue 2 Pg. 176-183 (11 2017) ISSN: 1521-0103 [Electronic] United States
• PMID: 28855373 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2017 by The American Society for Pharmacology and Experimental Therapeutics.

Chemical References

• Calcium-Calmodulin-Dependent Protein Kinase Type 2

Topics

• Animals
• Bone Neoplasms (complications)
• Calcium-Calmodulin-Dependent Protein Kinase Type 2 (metabolism)
• Chronic Pain (enzymology, etiology, pathology)
• Humans
• Neuralgia (enzymology, pathology)