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作 者:Shuang Zhu Bing-Sheng Yang Si-Jing Li Ge Tong Jian-Ye Tan Guo-Feng Wu Lin Li Guo-Li Chen Qian Chen Li-Jun Lin
机构地区:[1]Department of Joint and Orthopedics,Zhujiang Hospital,Southern Medical University,Guangzhou,Guangdong Province,China [2]Department of Medical Ultrasonics,Guangdong Province Key Laboratory of Hepatology Research,The Third Affiliated Hospital of Sun Yat-sen University,Guangzhou,Guangdong Province,China [3]Department of Orthopedics,Affiliated Hospital of Putian University,Putian,Fujian Province,China [4]Cell and Molecular Biology Laboratory,Department of Orthopaedics,Alpert Medical School of Brown University/Rhode Island Hospital,Providence,RI,USA
出 处:《Neural Regeneration Research》2021年第10期1935-1943,共9页中国神经再生研究(英文版)
基 金:This work was supported by the National Natural Science Foundation of China,No.81801210(to SZ).
摘 要:Deficits in intrinsic neuronal capacities in the spinal cord,a lack of growth support,and suppression of axonal outgrowth by inhibitory molecules mean that spinal cord injury almost always has devastating consequences.As such,one of the primary targets for the treatment of spinal cord injury is to develop strategies to antagonize extrinsic or intrinsic axonal growth-inhibitory factors or enhance the factors that support axonal growth.Among these factors,a series of individual protein level disorders have been identified during the generation of axons following spinal cord injury.Moreover,an increasing number of studies have indicated that post-translational modifications of these proteins have important implications for axonal growth.Some researchers have discovered a variety of post-translational modifications after spinal cord injury,such as tyrosination,acetylation,and phosphorylation.In this review,we reviewed the post-translational modifications for axonal growth,functional recovery,and neuropathic pain after spinal cord injury,a better understanding of which may elucidate the dynamic change of spinal cord injury-related molecules and facilitate the development of a new therapeutic strategy for spinal cord injury.
关 键 词:extracellular matrix function impairment glial scar nerve regeneration neuropathic pain post-translational modification spinal cord injury therapeutic target
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