Role of calmodulin kinase II in neuropathic pain and its pathway of pain regulation
Received:December 11, 2018  
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DOI:10. 3969 / j.issn.1005-4847. 2019. 03. 018
KeyWord:Ca2+ / calmodulin-dependent protein kinase; neuropathic pain; research progress
                    
AuthorInstitution
邰昭霞 1. 浙江中医药大学第三临床医学院,杭州 ; 2. 浙江省针灸神经病学研究重点实验室,杭州 ;3. 浙江中医药大学针灸研究所,杭州
费雪瑜 1. 浙江中医药大学第三临床医学院,杭州 ; 2. 浙江省针灸神经病学研究重点实验室,杭州 ;3. 浙江中医药大学针灸研究所,杭州
何晓芬 1. 浙江中医药大学第三临床医学院,杭州 ; 2. 浙江省针灸神经病学研究重点实验室,杭州 ;3. 浙江中医药大学针灸研究所,杭州
瞿思颖 浙江中医药大学第三临床医学院,杭州
王涵芝 浙江中医药大学第三临床医学院,杭州
方剑乔 1. 浙江中医药大学第三临床医学院,杭州 ; 2. 浙江省针灸神经病学研究重点实验室,杭州 ;3. 浙江中医药大学针灸研究所,杭州
蒋永亮 1. 浙江中医药大学第三临床医学院,杭州 ; 2. 浙江省针灸神经病学研究重点实验室,杭州 ;3. 浙江中医药大学针灸研究所,杭州
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Abstract:
      Ca2+ / calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/ threonine proteinkinase in a large number of neurons and is widely involved in pain modulation. Neuropathic pain is chronic refractory paincaused by disease or damage to the somatosensory system. CaMKII plays an important role in the occurrence anddevelopment of various types of neuropathic pain such as central, peripheral, diabetic and drug-induced neuropathic pain.This review focuses on the regulation of CaMKII-mediated neuropathic pain and its upstream and downstream pathways to provide a reference for the future study of CaMKII in the field of neuropathic pain.
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