Evidence map›Paper›PMID 23107876›Full record

ReviewJournal of cardiovascular pharmacology2013

Endothelial small-conductance and intermediate-conductance KCa channels: an update on their pharmacology and usefulness as cardiovascular targets.

Heike Wulff, Ralf Köhler

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 93 citations in OpenAlex.

  1. Metabolic Stress Shifts the Function of KArchiv der Pharmazie · 2026
    Article
  2. Review
  3. Article
  4. KJournal of neuroscience research · 2023
    Review
  5. Reduction of CaCells · 2023
    Article
  6. KBiomedicines · 2023
    Review
  7. Review
  8. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  9. CaMolecules (Basel, Switzerland) · 2023
    Review
  10. Review
  11. Allosteric inhibitors targeting the calmodulin-PIP2 interface of SK4 KProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Subtype-Selective Positive Modulation of KACS chemical biology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Endothelial Dysfunction in Primary Aldosteronism.International journal of molecular sciences · 2019
    Review
  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

2 authors at 2 institutions in 3 countries.

Heike WulffDepartment of Pharmacology, University of California, Davis, CA 95616, USA. hwulff@ucdavis.edu
Ralf Köhler
University of California, Davis · USUniversity of Southern Denmark · DK

Funding

The microglial potassium channels Kv1.3 and KCa3.1 as therapeutic targets for neuR01GM076063 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2006 to 2014
$2.5M
Optimization of KCa2 Channel Activators as Neuroscience Tools and Potential DrugsR21NS072585 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2011 to 2012
$440k
NIGMS NIH HHS R01 GM076063NIGMS NIH HHS R01GM076063NINDS NIH HHS R21 NS072585NINDS NIH HHS R21NS072585
6 · The paper itself

Abstract

Most cardiovascular researchers are familiar with intermediate-conductance KCa3.1 and small-conductance KCa2.3 channels because of their contribution to endothelium-derived hyperpolarization. However, to immunologists and neuroscientists, these channels are primarily known for their role in lymphocyte activation and neuronal excitability. KCa3.1 is involved in the proliferation and migration of T cells, B cells, mast cells, macrophages, fibroblasts, and dedifferentiated vascular smooth muscle cells and is, therefore, being pursued as a potential target for use in asthma, immunosuppression, and fibroproliferative disorders. In contrast, the 3 KCa2 channels (KCa2.1, KCa2.2, and KCa2.3) contribute to the neuronal medium afterhyperpolarization and, depending on the type of neuron, are involved in determining firing rates and frequencies or in regulating bursting. KCa2 activators are accordingly being studied as potential therapeutics for ataxia and epilepsy, whereas KCa2 channel inhibitors like apamin have long been known to improve learning and memory in rodents. Given this background, we review the recent discoveries of novel KCa3.1 and KCa2.3 modulators and critically assess the potential of KCa activators for the treatment of diabetes and cardiovascular diseases by improving endothelium-derived hyperpolarizations.

Indexed as

AnimalsBiological FactorsCardiovascular DiseasesDiabetes MellitusDrug DesignEndothelium, VascularHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsMolecular Targeted TherapySmall-Conductance Calcium-Activated Potassium ChannelsBiological Factorsendothelium-dependent hyperpolarization factorIntermediate-Conductance Calcium-Activated Potassium ChannelsSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID23107876
PMCPMC3565027
OpenAlexW2020460437

What OpenQuestion holds

Textmetadata
LicenceTDM
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.