Evidence map›Paper›PMID 25052376›Full record

ReviewCellular and molecular life sciences : CMLS2014

Ionic mechanisms in pancreatic β cell signaling.

Shao-Nian Yang, Yue Shi, Guang Yang, Yuxin Li, Jia Yu, Per-Olof Berggren

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Postnatal refinement of CaChannels (Austin, Tex.) · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Expression, localization and regulation of NADPH oxidases in pancreatic beta cells.Redox report : communications in free radical research · 2025
    Article
  7. Article
  8. The First KToxins · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. In Vivo CaBiomedicines · 2023
    Article
  16. A Review ofMolecules (Basel, Switzerland) · 2023
    Review
  17. Article
  18. Review
  19. Article
  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

6 authors at 3 institutions in 2 countries.

Shao-Nian YangThe Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden, shao-nian.yang@ki.se.
Yue Shi
Guang Yang
Yuxin Li
Jia Yu
Per-Olof Berggren
Karolinska Institutet · SEJilin Academy of Traditional Chinese Medicine · CNNortheast Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The function and survival of pancreatic β cells critically rely on complex electrical signaling systems composed of a series of ionic events, namely fluxes of K(+), Na(+), Ca(2+) and Cl(-) across the β cell membranes. These electrical signaling systems not only sense events occurring in the extracellular space and intracellular milieu of pancreatic islet cells, but also control different β cell activities, most notably glucose-stimulated insulin secretion. Three major ion fluxes including K(+) efflux through ATP-sensitive K(+) (KATP) channels, the voltage-gated Ca(2+) (CaV) channel-mediated Ca(2+) influx and K(+) efflux through voltage-gated K(+) (KV) channels operate in the β cell. These ion fluxes set the resting membrane potential and the shape, rate and pattern of firing of action potentials under different metabolic conditions. The KATP channel-mediated K(+) efflux determines the resting membrane potential and keeps the excitability of the β cell at low levels. Ca(2+) influx through CaV1 channels, a major type of β cell CaV channels, causes the upstroke or depolarization phase of the action potential and regulates a wide range of β cell functions including the most elementary β cell function, insulin secretion. K(+) efflux mediated by KV2.1 delayed rectifier K(+) channels, a predominant form of β cell KV channels, brings about the downstroke or repolarization phase of the action potential, which acts as a brake for insulin secretion owing to shutting down the CaV channel-mediated Ca(2+) entry. These three ion channel-mediated ion fluxes are the most important ionic events in β cell signaling. This review concisely discusses various ionic mechanisms in β cell signaling and highlights KATP channel-, CaV1 channel- and KV2.1 channel-mediated ion fluxes.

Indexed as

Signal TransductionAction PotentialsAdenosine TriphosphateAnimalsCalciumCalcium ChannelsCell MembraneExocytosisHumansInsulinInsulin-Secreting CellsIonsMembrane PotentialsPotassiumPotassium ChannelsAdenosine TriphosphateCalciumCalcium ChannelsInsulinIonsPotassiumPotassium Channels

Identifiers

PMID25052376
PMCPMC11113777
OpenAlexW2027739131

What Socratic 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 Socratic graph.