Traumatic brain injury （TBI） is a leading cause of death and disability worldwide. The finding that cellular microparticles （MPs） generated by injured cells profoundly impact on pathological courses of TBI has pav...Traumatic brain injury （TBI） is a leading cause of death and disability worldwide. The finding that cellular microparticles （MPs） generated by injured cells profoundly impact on pathological courses of TBI has paved the way for new diagnostic and therapeutic strategies. MPs are subcellular fragments or organelles that serve as carriers of lipids, adhesive receptors, cytokines, nucleic acids, and tissue-degrading enzymes that are unique to the parental cells. Their sub-micron sizes allow MPs to travel to areas that parental cells are unable to reach to exercise diverse biological functions. In this review, we summarize recent developments in identifying a casual role of MPs in the pathologies of TBI and suggest that MPs serve as a new class of therapeutic targets for the prevention and treatment of TBI and associated systemic complications.展开更多
Traumatic brain injury(TBI)is recognized as a global health problem due to its increasing occurrence,challenging treatment,and persistent impacts on brain pathophysiology.Neural cell death in patients with TBI swiftly...Traumatic brain injury(TBI)is recognized as a global health problem due to its increasing occurrence,challenging treatment,and persistent impacts on brain pathophysiology.Neural cell death in patients with TBI swiftly causes inflammation in the injured brain areas,which is recognized as focal brain inflammation.Focal brain inflammation causes secondary brain injury by exacerbating brain edema and neuronal death,while also exerting divergent beneficial effects,such as sealing the damaged limitans and removing cellular debris.Recent evidence from patients with TBI and studies on animal models suggest that brain inflammation after TBI is not only restricted to the focal lesion but also disseminates to remote areas of the brain.The dissemination of inflammation has been detected within days after the primary injury and persists chronically.This state of inflammation may be related to remote complications of TBI in patients,such as hyperthermia and hypopituitarism,and may lead to progressive neurodegeneration,such as chronic traumatic encephalopathy.Future studies should focus on understanding the mechanisms that govern the initiation and propagation of brain inflammation after TBI and its impacts on post-trauma brain pathology.展开更多
基金This study is supported by NIH grants NS087296 and HL71895 （JFD）, National Natural Science Foundation of China State Key Program Grant 81330029 and National Natural Science Foundation of China research Grants 81271361,81271359 （JNZ） and 81601068 （ZLZ）.
文摘Traumatic brain injury （TBI） is a leading cause of death and disability worldwide. The finding that cellular microparticles （MPs） generated by injured cells profoundly impact on pathological courses of TBI has paved the way for new diagnostic and therapeutic strategies. MPs are subcellular fragments or organelles that serve as carriers of lipids, adhesive receptors, cytokines, nucleic acids, and tissue-degrading enzymes that are unique to the parental cells. Their sub-micron sizes allow MPs to travel to areas that parental cells are unable to reach to exercise diverse biological functions. In this review, we summarize recent developments in identifying a casual role of MPs in the pathologies of TBI and suggest that MPs serve as a new class of therapeutic targets for the prevention and treatment of TBI and associated systemic complications.
基金supported in part by grants from the National Science Foundation of China(Grant numbers 81720108015,91642205,and 81830038)National Key Research and Development Program of China(2018YFC1312200)+1 种基金Tianjin Municipal Science and Technology Commission(15ZXLCSY00060)funds from the Advanced Innovation Center for Human Brain Protection,Capital Medical University,Beijing,China,and Barrow Neurological Foundation.
文摘Traumatic brain injury(TBI)is recognized as a global health problem due to its increasing occurrence,challenging treatment,and persistent impacts on brain pathophysiology.Neural cell death in patients with TBI swiftly causes inflammation in the injured brain areas,which is recognized as focal brain inflammation.Focal brain inflammation causes secondary brain injury by exacerbating brain edema and neuronal death,while also exerting divergent beneficial effects,such as sealing the damaged limitans and removing cellular debris.Recent evidence from patients with TBI and studies on animal models suggest that brain inflammation after TBI is not only restricted to the focal lesion but also disseminates to remote areas of the brain.The dissemination of inflammation has been detected within days after the primary injury and persists chronically.This state of inflammation may be related to remote complications of TBI in patients,such as hyperthermia and hypopituitarism,and may lead to progressive neurodegeneration,such as chronic traumatic encephalopathy.Future studies should focus on understanding the mechanisms that govern the initiation and propagation of brain inflammation after TBI and its impacts on post-trauma brain pathology.
