Autophagy in neuroinflammation after traumatic brain injury  

作　　者：Chinmoy Sarkar Marta M.Lipinski 

机构地区：[1]Shock,Trauma and Anesthesiology Research(STAR)Center,Department of Anesthesiology,University of Maryland School of Medicine,Baltimore,MD,USA [2]Department of Anatomy and Neurobiology,University of Maryland School of Medicine,Baltimore,MD,USA

出　　处：《Neural Regeneration Research》2024年第5期951-952,共2页中国神经再生研究（英文版）

基　　金：supported by NIH funding(R01NS091218 and R01NS115876)to MML.

摘　　要：Traumatic brain injury(TBI)is an acquired injury of the brain caused by the impact of external forces on the brain(Maas et al.,2008).It is a major cause of death and disability among people of all ages(Maas et al.,2008).The primary mechanical injury to the brain initiates a cascade of secondary biochemical events that lead to acute and chronic neurodegeneration and activation of inflammatory pathways(Maas et al.,2008).Both brain-resident microglia and blood-derived myeloid cells-macrophages and monocytes that infiltrate the brain due to injury-induced blood-brain barrier damage,contribute to the inflammatory responses after TBI(Morganti et al.,2015).

关 键 词：DAMAGE DEATH AFTER 

分 类 号：R651.15[医药卫生—外科学]