Evidence map›Paper›PMID 23430260›Full record

ArticleThe Journal of biological chemistry2013

Mitochondrial small conductance SK2 channels prevent glutamate-induced oxytosis and mitochondrial dysfunction.

Amalia M Dolga, Michael F Netter, Fabiana Perocchi, Nunzianna Doti, Lilja Meissner, Svenja Tobaben, Julia Grohm, Hans Zischka, Nikolaus Plesnila, Niels Decher and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

53 citing papers in PubMed, 95 citations in OpenAlex.

  1. SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Trial
  2. Small-conductance CaThe Journal of physiology · 2026
    Review
  3. Restoration of mitochondrial CaJournal of molecular and cellular cardiology · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Small-conductance calcium-activated potassium channels in the heart: expression, regulation and pathological implications.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Mitochondrial potassium channels: A novel calcitriol target.Cellular & molecular biology letters · 2022
    Article
  15. Review
  16. Article
  17. Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021
    Review
  18. Review
  19. Review
  20. Review
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

11 authors at 4 institutions in 5 countries.

Amalia M DolgaInstitut für Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universität Marburg, D-35032 Marburg, Germany. dolga@staff.uni-marburg.de
Michael F Netter
Fabiana Perocchi
Nunzianna Doti
Lilja Meissner
Svenja Tobaben
Julia Grohm
Hans Zischka
Nikolaus Plesnila
Niels Decher
Carsten Culmsee
Philipps University of Marburg · DERoyal College of Surgeons in Ireland · IEHarvard University · USHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small conductance calcium-activated potassium (SK2/K(Ca)2.2) channels are known to be located in the neuronal plasma membrane where they provide feedback control of NMDA receptor activity. Here, we provide evidence that SK2 channels are also located in the inner mitochondrial membrane of neuronal mitochondria. Patch clamp recordings in isolated mitoplasts suggest insertion into the inner mitochondrial membrane with the C and N termini facing the intermembrane space. Activation of SK channels increased mitochondrial K(+) currents, whereas channel inhibition attenuated these currents. In a model of glutamate toxicity, activation of SK2 channels attenuated the loss of the mitochondrial transmembrane potential, blocked mitochondrial fission, prevented the release of proapoptotic mitochondrial proteins, and reduced cell death. Neuroprotection was blocked by specific SK2 inhibitory peptides and siRNA targeting SK2 channels. Activation of mitochondrial SK2 channels may therefore represent promising targets for neuroprotective strategies in conditions of mitochondrial dysfunction.

Indexed as

AnimalsCell LineCell MembraneGlutamic AcidMembrane Potential, MitochondrialMiceMitochondriaMitochondrial MembranesNerve Tissue ProteinsNeuronsNeuroprotective AgentsPeptidesPotassiumSmall-Conductance Calcium-Activated Potassium ChannelsGlutamic AcidKcnn2 protein, mouseNerve Tissue ProteinsNeuroprotective AgentsPeptidesPotassiumSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID23430260
PMCPMC3624460
OpenAlexW2128578535

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.