TY - JOUR T1 - Cellular and molecular mechanisms of calcium/calmodulin-dependent protein kinase II in chronic pain JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther DO - 10.1124/jpet.117.243048 SP - jpet.117.243048 AU - Ya-Qun Zhou AU - Dai-Qiang Liu AU - Shu-Ping Chen AU - Jia Sun AU - Xue-Rong Zhou AU - Fang Luo AU - Yu-Ke Tian AU - Da-Wei Ye Y1 - 2017/01/01 UR - http://jpet.aspetjournals.org/content/early/2017/08/31/jpet.117.243048.abstract N2 - Chronic pain, often defined as any pain lasting more than 3 months, is poorly managed due to its multifaceted and complex mechanisms. Calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinase, which plays a fundamental role in synaptic plasticity, learning and memory. Recently, emerging evidence demonstrate 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 strategy for the management of chronic pain in the future. ER -