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Therapeutic Targeting of Astrocytes After Traumatic Brain Injury

Scholary Output:
Contribution to journal
Review article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

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.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 633-642 (10 pages)

Journal (Volume, Issue Number)

Translational Stroke Research (Volume 2, Issue 4)

Publication milestones

  • Published - 12/2011

Publication status

Published - 12/2011

ISSN

1868-4483

Publication IDs

  • Scopus: 83355163225
  • PubMed: 24323684

Publication metrics

Metrics

Scopus
citations
SciVal
citations
13
Fractional count
3
Fractional count
0.50
Fractional count
3
Fractional count
0.50
Fractional count
3
Fractional count
1
SciVal
FWCI
0.12
SciVal
Author count
6
SciVal
Paper percentile
69

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Citation count
15
Captures
22

Funding Details

Acknowledgments The authors’ work is supported in part by grants from the National Institute of Health (NS065172) and American Heart Association (BGIA2300135).
FundersFunding numbers
NIH
NS065172
AHA
BGIA2300135