文献类型：期刊文献

英文题名：Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury

作者：Lu, Qicheng[1];Zhang, Yong[1];Botchway, Benson O. A.[2,3];Huang, Min[1];Liu, Xuehong[1]

机构：[1]Shaoxing Univ, Med Coll, Dept Histol & Embryol, Shaoxing 312000, Zhejiang, Peoples R China;[2]Zhejiang Univ, Inst Neurosci, Sch Med, Hangzhou, Peoples R China;[3]Bupa Cromwell Hosp, London, England

年份：2023

外文期刊名：MOLECULAR NEUROBIOLOGY

收录：SCI-EXPANDED(收录号：WOS:001033509900003)、、Scopus(收录号：2-s2.0-85164963020)、WOS

语种：英文

外文关键词：Syntaphilin (Snph); Mitochondrial transport; Spinal cord injury (SCI); Axon regeneration; P21 activated kinase 5 (PAK5); Akt-PAK5 signaling

外文摘要：Mitochondria are important organelle of eukaryotic cells. They consists of a large number of different proteins that provide most of the ATP and supply power for the growth, function, and regeneration of neurons. Therefore, smitochondrial transport ensures that adequate ATP is supplied for metabolic activities. Spinal cord injury (SCI), a detrimental condition, has high morbidity and mortality rates. Currently, the available treatments only provide symptomatic relief for long-term disabilities. Studies have implicated mitochondrial transport as a critical factor in axonal regeneration. Hence, enhancing mitochondrial transports could be beneficial for ameliorating SCI. Syntaphilin (Snph) is a mitochondrial docking protein that acts as a "static anchor," and its inhibition enhances mitochondrial transports. Therefore, Snph as a key mediator of mitochondrial transports, may contribute to improving axonal regeneration following SCI. Herein, we examine Snph's biological effects and its relation to mitochondrial pathway. Then, we elaborate on mitochondrial transports after SCI, the possible role of Snph in SCI, and some possible therapeutic approaches by Snph.