Evidence map›Paper›PMID 25749474›Full record

ReviewInternational journal of molecular sciences2015

Glibenclamide for the treatment of ischemic and hemorrhagic stroke.

Nicholas Caffes, David B Kurland, Volodymyr Gerzanich, J Marc Simard

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.

  1. Sulfonylurea drugs for people with severe hemispheric ischemic stroke.The Cochrane database of systematic reviews · 2025
    Pooled it
  2. Pooled it
  3. Trial
  4. Cerebrovascular effects of glibenclamide investigated using high-resolution magnetic resonance imaging in healthy volunteers.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Trial
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. A new perspective on cerebrospinal fluid dynamics after subarachnoid hemorrhage: From normal physiology to pathophysiological changes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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.

Nicholas CaffesDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA. nicholas.caffes@som.umaryland.edu.
David B KurlandDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA. kurland.davidb@gmail.com.
Volodymyr GerzanichDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA. vgerzanich@smail.umaryland.edu.
J Marc SimardDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA. msimard@smail.umaryland.edu.
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
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
NHLBI NIH HHS HL082517NHLBI NIH HHS R01 HL082517NINDS NIH HHS NS061808NINDS NIH HHS R01 NS061808
6 · The paper itself

Abstract

Ischemic and hemorrhagic strokes are associated with severe functional disability and high mortality. Except for recombinant tissue plasminogen activator, therapies targeting the underlying pathophysiology of central nervous system (CNS) ischemia and hemorrhage are strikingly lacking. Sur1-regulated channels play essential roles in necrotic cell death and cerebral edema following ischemic insults, and in neuroinflammation after hemorrhagic injuries. Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1-transient receptor potential melastatin 4 (Sur1-Trpm4) channels and, in some cases, microglial KATP (Sur1-Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Robust preclinical studies have shown that glibenclamide and other sulfonylurea agents reduce infarct volumes, edema and hemorrhagic conversion, and improve outcomes in rodent models of ischemic stroke. Retrospective studies suggest that diabetic patients on sulfonylurea drugs at stroke presentation fare better if they continue on drug. Additional laboratory investigations have implicated Sur1 in the pathophysiology of hemorrhagic CNS insults. In clinically relevant models of subarachnoid hemorrhage, glibenclamide reduces adverse neuroinflammatory and behavioral outcomes. Here, we provide an overview of the preclinical studies of glibenclamide therapy for CNS ischemia and hemorrhage, discuss the available data from clinical investigations, and conclude with promising preclinical results that suggest glibenclamide may be an effective therapeutic option for ischemic and hemorrhagic stroke.

Indexed as

AnimalsBlood-Brain BarrierGlyburideHumansHypoglycemic AgentsKATP ChannelsStrokeSulfonylurea ReceptorsABCC8 protein, humanGlyburideHypoglycemic AgentsKATP ChannelsSulfonylurea Receptors

Identifiers

PMID25749474
PMCPMC4394459
OpenAlexW2148056291

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.