Evidence map›Paper›PMID 25873902›Full record

ReviewFrontiers in physiology2015

Mitochondrial BKCa channel.

Enrique Balderas, Jin Zhang, Enrico Stefani, Ligia Toro

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.2field-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

49 citing papers in PubMed, 96 citations in OpenAlex.

  1. BKJournal of neuro-oncology · 2026
    Article
  2. Small-conductance CaThe Journal of physiology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Regulatory mechanisms of mitochondrial BKChannels (Austin, Tex.) · 2021
    Review
  17. Review
  18. Identification of the Large-Conductance CaMolecules (Basel, Switzerland) · 2021
    Article
  19. Review
  20. Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    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.

Enrique BalderasDepartment of Anesthesiology, University of California, Los Angeles Los Angeles, CA, USA.
Jin ZhangDeparment of Molecular and Medical Pharmacology, University of California, Los Angeles Los Angeles, CA, USA.
Enrico StefaniDepartment of Anesthesiology, University of California, Los Angeles Los Angeles, CA, USA ; Department of Physiology, University of California, Los Angeles Los Angeles, CA, USA ; Brain Research Institute, University of California, Los Angeles Los Angeles, CA, USA ; Cardiovascular Research Laboratory, University of California, Los Angeles Los Angeles, CA, USA.
Ligia ToroDepartment of Anesthesiology, University of California, Los Angeles Los Angeles, CA, USA ; Deparment of Molecular and Medical Pharmacology, University of California, Los Angeles Los Angeles, CA, USA ; Brain Research Institute, University of California, Los Angeles Los Angeles, CA, USA ; Cardiovascular Research Laboratory, University of California, Los Angeles Los Angeles, CA, USA.
University of California, Los Angeles · US

Funding

BK(Ca) channel in heart mitochondriaR01HL107418 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI OLCESE, RICCARDO, STEFANI, ENRICO · 2012 to 2015
$2.5M
NHLBI NIH HHS R01 HL107418
6 · The paper itself

Abstract

Since its discovery in a glioma cell line 15 years ago, mitochondrial BKCa channel (mitoBKCa) has been studied in brain cells and cardiomyocytes sharing general biophysical properties such as high K(+) conductance (~300 pS), voltage-dependency and Ca(2+)-sensitivity. Main advances in deciphering the molecular composition of mitoBKCa have included establishing that it is encoded by the Kcnma1 gene, that a C-terminal splice insert confers mitoBKCa ability to be targeted to cardiac mitochondria, and evidence for its potential coassembly with β subunits. Notoriously, β1 subunit directly interacts with cytochrome c oxidase and mitoBKCa can be modulated by substrates of the respiratory chain. mitoBKCa channel has a central role in protecting the heart from ischemia, where pharmacological activation of the channel impacts the generation of reactive oxygen species and mitochondrial Ca(2+) preventing cell death likely by impeding uncontrolled opening of the mitochondrial transition pore. Supporting this view, inhibition of mitoBKCa with Iberiotoxin, enhances cytochrome c release from glioma mitochondria. Many tantalizing questions remain open. Some of them are: how is mitoBKCa coupled to the respiratory chain? Does mitoBKCa play non-conduction roles in mitochondria physiology? Which are the functional partners of mitoBKCa? What are the roles of mitoBKCa in other cell types? Answers to these questions are essential to define the impact of mitoBKCa channel in mitochondria biology and disease.

Indexed as

BK channelsischemia reperfusion injuryMaxiK channelsmitochondriapermeability transition porepotassium channelssubunit composition

Identifiers

PMID25873902
PMCPMC4379900
OpenAlexW1977659817

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.