Evidence map›Paper›PMID 23272793›Full record

ReviewExpert review of clinical pharmacology2013

KCNE genetics and pharmacogenomics in cardiac arrhythmias: much ado about nothing?

Geoffrey W Abbott

Abstract readReview
In one paragraph

Review in Expert review of clinical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Insights into Cardiac IKs (KCNQ1/KCNE1) Channels Regulation.International journal of molecular sciences · 2020
    Review
  7. Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Kcne3 deletion initiates extracardiac arrhythmogenesis in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    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

1 author at 1 institution in 1 country.

Geoffrey W AbbottDepartment of Pharmacology, Department of Physiology & Biophysics, University of California, Irvine, CA, USA. abbottg@uci.edu
University of California, Irvine · US

Funding

K+ channel trafficking and modulation in MinK and MiRP1R01HL079275 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ABBOTT, GEOFFREY W · 2005 to 2015
$4.6M
Predictive multiscale modeling of atrial fibrillation for therapy developmentR01HL101190 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI ABBOTT, GEOFFREY W, CHRISTINI, DAVID J. · 2010 to 2013
$1.7M
NHLBI NIH HHS HL079275NHLBI NIH HHS HL101190NHLBI NIH HHS R01 HL079275NHLBI NIH HHS R01 HL101190
6 · The paper itself

Abstract

Voltage-gated ion channels respond to changes in membrane potential with conformational shifts that either facilitate or stem the movement of charged ions across the cell membrane. This controlled movement of ions is particularly important for the action potentials of excitable cells such as cardiac myocytes and therefore essential for timely beating of the heart. Inherited mutations in ion channel genes and in the genes encoding proteins that regulate them can cause lethal cardiac arrhythmias either by direct channel disruption or by altering interactions with therapeutic drugs, the best-understood example of both these scenarios being long QT syndrome (LQTS). Unsurprisingly, mutations in the genes encoding ion channel pore-forming α subunits underlie the large majority (~90%) of identified cases of inherited LQTS. Given that inherited LQTS is comparatively rare in itself (~0.04% of the US population), is pursuing study of the remaining known and unknown LQTS-associated genes subject to the law of diminishing returns? Here, with a particular focus on the KCNE family of single transmembrane domain K(+) channel ancillary subunits, the significance to cardiac pharmacogenetics of ion channel regulatory subunits is discussed.

Indexed as

PharmacogeneticsArrhythmias, CardiacHumansLong QT SyndromeMembrane PotentialsMutationPotassium Channels, Voltage-GatedPotassium Channels, Voltage-Gated

Identifiers

PMID23272793
PMCPMC4917007
OpenAlexW1964978052

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.