A lead role for a“secondary”axonal injury response  

作　　者：Melissa A.Rudy Trent A.Watkins 

机构地区：[1]Division of Neuroimmunology and Glial Biology,Department of Neurology,University of California at San Francisco,San Francisco,CA,USA [2]Development,Disease Models,and Therapeutics Graduate Program,Baylor College of Medicine,Houston,TX,USA

出　　处：《Neural Regeneration Research》2025年第2期469-470,共2页中国神经再生研究（英文版）

基　　金：supported by grants from Mission Connect, a project of the TIRR Foundation, the Glaucoma Research Foundation;NIH grants R01NS112691 and R01NS076708 (to TAW)

摘　　要：Stress signaling following axon injury stimulates a transcriptional program for regeneration that might be exploited to promote central nervous system repair.However,this stress response drives neuronal apoptosis in non-regenerative environments.This duality presents a quandary for the development of therapeutic interventions:manipulating stress signaling to enhance recovery of damaged neurons risks accelerating neurodegeneration or restricting regenerative potential.This dichotomy is well illustrated by the fates of retinal ganglion cells(RGCs)following optic nerve crush.In this central nervous system injury model,disruption of a stress-activated MAP kinase(MAPK)cascade blocks the extensive apoptosis of RGCs that occurs in wild-type mice(Watkins et al.,2013;Welsbie et al.,2017).

关 键 词：INJURY AXONAL STRESS 

分 类 号：R338[医药卫生—人体生理学]