Cell Metabolism . . . The joint research results of the Xu Xiaoming/Sheng Zuhang team have improved energy supply to help restore spinal cord injury.

One of the main characteristics of nemei spinal cord injury is the damage of the upper and lower nerve conduction tracts that control movement and sensation in the spinal cord, which leads to the dysfunction of body movement and sensation. Therefore, promoting the regeneration of central nerve fibers or axons and reconstituting synaptic connections with the innervated neurons are the neurobiological basis of functional recovery after spinal cord injury.however, after spinal cord injury, the inhibitory external microenvironment and the loss of regeneration ability of central neurons after spinal cord injury lead to the failure of axonal regeneration after spinal cord injury.therefore, central nerve regeneration is still an important problem in the field of medical research in the world.recently, the Xu Xiaoming research group of the school of medicine of Indiana University and Sheng zuhang research group of the National Institutes of health of the United States (the first author, Dr. Han Qi) published a research paper entitled "restoring cellular energy promoters axial regeneration and functional recovery after spinal cord injury" in cell metabolism.this study found that increasing the energy supply of neurons can promote nerve regeneration and functional recovery after spinal cord injury.to solve this important problem, Xu Xiaoming and Sheng zuhang team cooperated closely. They first used synthaphilin knockout mice to study the relationship between mitochondrial transport and nerve regeneration in axons.the protein receptor expressed by syntaphilin gene can anchor mitochondria into axons.this protein is expressed in a large number of mature neurons, which slows down the mitochondrial transport speed of axons.when the researchers genetically removed synapphilin from nerve cells, mitochondrial transport was enhanced.the research group found that the syntaphilin gene knockout mice with rapid mitochondrial transport can replace and repair the damaged mitochondria after spinal cord injury more quickly, thus producing more energy, namely ATP.by removing the mitochondrial anchor protein synthaphilin (snph) from nerve cells, the transport efficiency of mitochondria in axons was increased, or creatine in neurons was supplied by exogenous The contents of creatine and creatine phosphate can increase the energy supply of damaged neurons, thus promoting axonal regeneration, nerve circuit reconstruction and motor function recovery after spinal cord injury.through three different spinal cord injury models, the research group revealed that in different types of spinal cord injury, the enhancement of ATP is very important for axon regeneration of different central nerve conduction tracts, neural circuit remodeling and motor function recovery of spinal cord.the researchers also found that increasing the level of creatine or creatine phosphate metabolism in neurons can quickly restore the number of ATP and promote axonal regeneration.these results demonstrate for the first time the importance of energy reserve of nerve cells in nerve regeneration after spinal cord injury.highly differentiated neurons are under the pressure of extreme energy loss after injury. This study shows that enhancing the transport of mitochondria in axons or improving energy metabolism plays a key role in promoting axonal regeneration and functional recovery of the central nervous system.this discovery not only provides a new idea and research direction for the basic research of nerve regeneration after spinal cord injury, but also has high feasibility of clinical transformation by improving energy metabolism to promote nerve regeneration.the follow-up project of the research team will deeply study the effective drugs regulating mitochondrial transport and metabolism, and how to promote long-distance axonal regeneration and functional recovery after spinal cord injury. original link: plate maker: Ke