Evidence map›Paper›PMID 8415718›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus.

C Heurteaux, V Bertaina, C Widmann, M Lazdunski

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 180 citations in OpenAlex.

  1. Article
  2. Selective block of adenosine ABritish journal of pharmacology · 2022
    Article
  3. Inhibition of eIF5A hypusination pathway as a new pharmacological target for stroke therapy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The role of KActa pharmacologica Sinica · 2018
    Review
  10. Alleviation by GABANeurochemical research · 2018
    Article
  11. Article
  12. Article
  13. Condition-specific transcriptional regulation of neuronal ion channel genes in brain ischemia.International journal of physiology, pathophysiology and pharmacology · 2017
    Article
  14. "New Old Pathologies": AD, PART, and Cerebral Age-Related TDP-43 With Sclerosis (CARTS).Journal of neuropathology and experimental neurology · 2016
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Up-regulation of A-type potassium currents protects neurons against cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011
    Article
  20. Traumatic brain injury in mice lacking the K channel, TREK-1.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011
    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.

C HeurteauxInstitut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France.
V Bertaina
C Widmann
M Lazdunski
Institut de Pharmacologie Moléculaire et Cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient global forebrain ischemia induces in rat brain a large increase of expression of the immediate early genes c-fos and c-jun and of the mRNAs for the 70-kDa heat-shock protein and for the form of the amyloid beta-protein precursor including the Kunitz-type protease-inhibitor domain. At 24 hr after ischemia, this increased expression is particularly observed in regions that are vulnerable to the deleterious effects of ischemia, such as pyramidal cells of the CA1 field in the hippocampus. In an attempt to find conditions which prevent the deleterious effects of ischemia, representatives of three different classes of K+ channel openers, (-)-cromakalim, nicorandil, and pinacidil, were administered both before ischemia and during the reperfusion period. This treatment totally blocked the ischemia-induced expression of the different genes. In addition it markedly protected neuronal cells against degeneration. The mechanism of the neuroprotective effects involves the opening of ATP-sensitive K+ channels since glipizide, a specific blocker of that type of channel, abolished the beneficial effects of K+ channel openers. The various classes of K+ channel openers seem to deserve attention as potential drugs for cerebral ischemia.

Indexed as

Alternative SplicingAmyloid beta-Protein PrecursorAnimalsBase SequenceBenzopyransBrain IschemiaCell DeathCromakalimGene Expression RegulationGuanidinesHeat-Shock ProteinsHippocampusIn Situ HybridizationMaleMolecular Sequence DataNeuronsAmyloid beta-Protein PrecursorBenzopyransCromakalimGuanidinesHeat-Shock ProteinsNiacinamideNicorandilOligonucleotide ProbesPinacidilPotassium ChannelsProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junPyrrolesRNA, Messenger

Identifiers

PMID8415718
PMCPMC47582
OpenAlexW2137083867

What OpenQuestion holds

Textmetadata
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.