Evidence map›Paper›PMID 24323720›Full record

ReviewTranslational stroke research2014

Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration.

Niyathi Hegde Shah, Elias Aizenman

Open access · greenAbstract readReview
In one paragraph

Review in Translational stroke research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Dynamic glycosylation remodeling in neurological disorders.Frontiers in molecular neuroscience · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Inhaled Anesthetics: Beyond the Operating Room.Journal of clinical medicine · 2024
    Review
  16. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  17. The involvement of KTranslational psychiatry · 2024
    Review
  18. Article
  19. Article
  20. Article

40 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

2 authors at 1 institution in 1 country.

Niyathi Hegde ShahDepartment of Neurobiology, University of Pittsburgh School of Medicine, 3500 Terrace Street, E1456 BST, Pittsburgh, PA, 15261, USA, ngh7@pitt.edu.
Elias Aizenman
University of Pittsburgh · US

Funding

Liberation of Intracellular Zinc and Neuronal Cell DeathR01NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2002 to 2022
$8.2M
A novel neuroprotective strategyR21NS078238 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2012 to 2013
$396k
Liberation of Intracellular Zinc and Neuronal Cell DeathR56NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2007 to 2007
$371k
NINDS NIH HHS NS043277NINDS NIH HHS R01 NS043277NINDS NIH HHS R21 NS078238NINDS NIH HHS R56 NS043277
6 · The paper itself

Abstract

Voltage-gated potassium (Kv) channels are widely expressed in the central and peripheral nervous system and are crucial mediators of neuronal excitability. Importantly, these channels also actively participate in cellular and molecular signaling pathways that regulate the life and death of neurons. Injury-mediated increased K(+) efflux through Kv2.1 channels promotes neuronal apoptosis, contributing to widespread neuronal loss in neurodegenerative disorders such as Alzheimer's disease and stroke. In contrast, some forms of neuronal activity can dramatically alter Kv2.1 channel phosphorylation levels and influence their localization. These changes are normally accompanied by modifications in channel voltage dependence, which may be neuroprotective within the context of ischemic injury. Kv1 and Kv7 channel dysfunction leads to neuronal hyperexcitability that critically contributes to the pathophysiology of human clinical disorders such as episodic ataxia and epilepsy. This review summarizes the neurotoxic, neuroprotective, and neuroregulatory roles of Kv channels and highlights the consequences of Kv channel dysfunction on neuronal physiology. The studies described in this review thus underscore the importance of normal Kv channel function in neurons and emphasize the therapeutic potential of targeting Kv channels in the treatment of a wide range of neurological diseases.

Indexed as

ApoptosisAnimalsBrain IschemiaHumansNeuronsPotassium Channels, Voltage-GatedPotassium Channels, Voltage-Gated

Identifiers

PMID24323720
PMCPMC3946373
OpenAlexW2022915497

What OpenQuestion holds

Textmetadata
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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.