Evidence map›Paper›PMID 24996934›Full record

ReviewNeurochemical research2015

Mechanisms of astrocyte-mediated cerebral edema.

Jesse A Stokum, David B Kurland, Volodymyr Gerzanich, J Marc Simard

Open access · greenAbstract readReview
In one paragraph

Review in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

97 citing papers in PubMed, 2 syntheses or guidelines pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Genetic ablation ofiScience · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Science advances · 2025
    Article
  12. Dialysis and cognitive impairment.Nature reviews. Nephrology · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jesse A StokumDepartment of Neurosurgery, University of Maryland School of Medicine, 22 S. Greene St., Suite S12D, Baltimore, MD, 21201-1595, USA.
David B Kurland
Volodymyr Gerzanich
J Marc Simard
University of Maryland, Baltimore · US

Funding

Sulfonylurea receptor 1 (SUR1)- A novel therapeutic target in ischemic strokeR01HL082517 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2006 to 2021
$5.6M
TRPM4 channel in spinal cord injuryR01NS061934 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2008 to 2018
$3.3M
Spinal cord injury, progressive hemorrhagic necrosis and the NC(Ca-ATP) channelR01NS060801 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2009 to 2018
$3.3M
Sur1-Trpm4 regulation of the pro-inflammatory astrocytic secretome in EAER01NS107262 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2020 to 2024
$1.7M
Pathological role of the SUR1-regulated NC(Ca-ATP) channel in cortex after subaraR01NS061808 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2009 to 2013
$1.6M
Role of TRP channels in secondary injury after brain traumaR01NS072501 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GERZANICH, VLADIMIR · 2011 to 2014
$1.3M
Brain injury due to transcranial versus transthoracic blast exposureI01BX001629 · VA · BALTIMORE VA MEDICAL CENTER · PI SIMARD, J. MARC · 2013 to 2016
–
BLRD VA I01 BX001629NHLBI NIH HHS HL082517NHLBI NIH HHS R01 HL082517NINDS NIH HHS NS060801NINDS NIH HHS NS061808NINDS NIH HHS NS061934NINDS NIH HHS NS072501NINDS NIH HHS R01 NS060801NINDS NIH HHS R01 NS061808NINDS NIH HHS R01 NS061934NINDS NIH HHS R01 NS072501NINDS NIH HHS R01 NS107262
6 · The paper itself

Abstract

Cerebral edema formation stems from disruption of blood brain barrier (BBB) integrity and occurs after injury to the CNS. Due to the restrictive skull, relatively small increases in brain volume can translate into impaired tissue perfusion and brain herniation. In excess, cerebral edema can be gravely harmful. Astrocytes are key participants in cerebral edema by virtue of their relationship with the cerebral vasculature, their unique compliment of solute and water transport proteins, and their general role in brain volume homeostasis. Following the discovery of aquaporins, passive conduits of water flow, aquaporin 4 (AQP4) was identified as the predominant astrocyte water channel. Normally, AQP4 is highly enriched at perivascular endfeet, the outermost layer of the BBB, whereas after injury, AQP4 expression disseminates to the entire astrocytic plasmalemma, a phenomenon termed dysregulation. Arguably, the most important role of AQP4 is to rapidly neutralize osmotic gradients generated by ionic transporters. In pathological conditions, AQP4 is believed to be intimately involved in the formation and clearance of cerebral edema. In this review, we discuss aquaporin function and localization in the BBB during health and injury, and we examine post-injury ionic events that modulate AQP4-dependent edema formation.

Indexed as

AnimalsAquaporin 4AstrocytesBlood-Brain BarrierBrain EdemaCell MembraneHumansAquaporin 4

Identifiers

PMID24996934
PMCPMC4284155
OpenAlexW2021036163

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.