Evidence map›Paper›PMID 22145034›Full record

ArticlePloS one2011

SLO-2 is cytoprotective and contributes to mitochondrial potassium transport.

Andrew P Wojtovich, Teresa A Sherman, Sergiy M Nadtochiy, William R Urciuoli, Paul S Brookes, Keith Nehrke

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-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

38 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Regulatory mechanisms of mitochondrial BKChannels (Austin, Tex.) · 2021
    Review
  6. Article
  7. Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance in C. elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  12. Review
  13. Pharmacological modulation of mitochondrial ion channels.British journal of pharmacology · 2019
    Review
  14. Cardiac metabolic effects of KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

6 authors at 1 institution in 1 country.

Andrew P WojtovichDepartment of Medicine, University of Rochester Medical Center, Rochester, New York, United States of America.
Teresa A Sherman
Sergiy M Nadtochiy
William R Urciuoli
Paul S Brookes
Keith Nehrke
University of Rochester Medical Center · US

Funding

SIRT1, Nitro-Lipids and CardioprotectionR01HL071158 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S · 2003 to 2025
$7.7M
Mitochondrial K+ Channels and CardioprotectionR01GM087483 · NIGMS · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S, NEHRKE, KEITH · 2010 to 2017
$2.3M
NHLBI NIH HHS HL071158NHLBI NIH HHS R01 HL071158NIGMS NIH HHS GM087483NIGMS NIH HHS R01 GM087483
6 · The paper itself

Abstract

Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance "big" K(+) channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposure to volatile anesthetics initiates protection against ischemic injury. Despite the role of the mBK in cardioprotection, the molecular identity of the channel remains unknown. We investigated the attributes of the mBK using C. elegans and mouse genetic models coupled with measurements of mitochondrial K(+) transport and APC. The canonical Ca(2+)-activated BK (or "maxi-K") channel SLO1 was dispensable for both mitochondrial K(+) transport and APC in both organisms. Instead, we found that the related but physiologically-distinct K(+) channel SLO2 was required, and that SLO2-dependent mitochondrial K(+) transport was triggered directly by volatile anesthetics. In addition, a SLO2 channel activator mimicked the protective effects of volatile anesthetics. These findings suggest that SLO2 contributes to protection from hypoxic injury by increasing the permeability of the mitochondrial inner membrane to K(+).

Indexed as

CytoprotectionIschemic Preconditioning, MyocardialAnesthetics, InhalationAnimalsCaenorhabditis elegans ProteinsHypoxiaImmunoblottingIndolesIon TransportLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMaleMembrane Potential, MitochondrialMembrane Transport ProteinsMiceMice, Inbred C57BLMice, KnockoutAnesthetics, InhalationCaenorhabditis elegans ProteinsIndolesKcnma1 protein, mouseLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane Transport ProteinspaxillinePotassium Channel BlockersSLO-2 protein, C elegans

Identifiers

PMID22145034
PMCPMC3228735
OpenAlexW1972091475

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.