TY - JOUR
T1 - Therapeutic Targeting of Astrocytes After Traumatic Brain Injury
AU - Shields, Jessica
AU - Kimbler, Donald E.
AU - Radwan, Walid
AU - Yanasak, Nathan
AU - Sukumari-Ramesh, Sangeetha
AU - Dhandapani, Krishnan M.
N1 - Funding Information:
Acknowledgments The authors’ work is supported in part by grants from the National Institute of Health (NS065172) and American Heart Association (BGIA2300135).
PY - 2011/12
Y1 - 2011/12
N2 - Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. A major focus of preclinical research has focused on understanding the mechanisms of acute cell death after TBI; however, translation of these findings into the clinic has failed to improve long-term patient outcomes. Recent work suggests astrocytes, the predominant cell type within the human brain, may actively contribute to neurological demise by exacerbating secondary brain injury after TBI. Along these lines, astrocytes may promote neuroinflammation, increase the development of cerebral edema, and contribute to elevated intracranial pressure after brain injury. The primary goal of this mini-review is to summarize the growing body of literature that suggests reactive astrocytes influence the brain response to TBI. To maintain focus, we will limit our discussion to the mechanisms of cerebral edema.
AB - Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. A major focus of preclinical research has focused on understanding the mechanisms of acute cell death after TBI; however, translation of these findings into the clinic has failed to improve long-term patient outcomes. Recent work suggests astrocytes, the predominant cell type within the human brain, may actively contribute to neurological demise by exacerbating secondary brain injury after TBI. Along these lines, astrocytes may promote neuroinflammation, increase the development of cerebral edema, and contribute to elevated intracranial pressure after brain injury. The primary goal of this mini-review is to summarize the growing body of literature that suggests reactive astrocytes influence the brain response to TBI. To maintain focus, we will limit our discussion to the mechanisms of cerebral edema.
KW - Aquaporin
KW - Cerebral blood flow
KW - ICP
KW - Inflammation
KW - Intracranial pressure
KW - Neurotrauma
UR - http://www.scopus.com/inward/record.url?scp=83355163225&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=83355163225&partnerID=8YFLogxK
U2 - 10.1007/s12975-011-0129-6
DO - 10.1007/s12975-011-0129-6
M3 - Review article
C2 - 24323684
AN - SCOPUS:83355163225
SN - 1868-4483
VL - 2
SP - 633
EP - 642
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - 4
ER -