A lead role for a"secondary"axonal injury response
Melissa A.Rudy1
Trent A.Watkins2
1.Division of Neuroimmunology and Glial Biology,Department of Neurology,University of California at San Francisco,San Francisco,CA,USA2.Division of Neuroimmunology and Glial Biology,Department of Neurology,University of California at San Francisco,San Francisco,CA,USA;Development,Disease Models,and Therapeutics Graduate Program,Baylor College of Medicine,Houston,TX,USA
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.
机标关键词：secondaryleadroleaxonalinjuryresponse
论文发表日期：2025-02-27
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 469-470 )