Evidence map›Paper›PMID 30598284›Full record

ArticleBiophysical journal2019

Propagation Failure by TRPM4 Overexpression.

Namit Gaur, Thomas Hof, Michel Haissaguerre, Edward J Vigmond

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Role of TRPM4 ion channel in pediatric arrhythmic syndromes.World journal of clinical pediatrics · 2026
    Review
  2. Review
  3. Review
  4. The Role of TRPM4 in Cardiac Electrophysiology and Arrhythmogenesis.International journal of molecular sciences · 2023
    Review
  5. Review
  6. Article
  7. CaHeliyon · 2020
    Article
  8. 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 3 institutions in 1 country.

Namit GaurUniversity Bordeaux, IMB UMR 5251, Talence, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France.
Thomas HofIHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France; Université Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, Bordeaux, France.
Michel HaissaguerreIHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France; Bordeaux University Hospital (CHU), Cardiac Electrophysiology and Cardiac Stimulation Team, Pessac, France.
Edward J VigmondUniversity Bordeaux, IMB UMR 5251, Talence, France; IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, Pessac-Bordeaux, France. Electronic address: edward.vigmond@u-bordeaux.fr.
Electrophysiology and Heart Modeling Institute · FRCentre de Recherche Cardio-Thoracique de Bordeaux · FRInstitut de Mathématiques de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential melastatin member 4 (TRPM4) channels are nonselective monovalent cationic channels found in human atria and conduction system. Overexpression of TRPM4 channels has been found in families suffering from inherited cardiac arrhythmias, notably heart block. In this study, we integrate a mathematical formulation of the TRPM4 channel into a Purkinje cell model (Pan-Rudy model). Instead of simply adding the channel to the model, a combination of existing currents equivalent to the TRPM4 current was constructed, based on TRPM4 current dynamics. The equivalent current was then replaced by the TRPM4 current to preserve the model action potential. Single-cell behavior showed early afterdepolarizations for increases in TRPM4 channel expression above twofold. In a homogeneous strand of tissue, propagation conducted faithfully for lower expression levels but failed completely for more than a doubling of TRPM4 channel expression. Only with a heterogeneous distribution of channel expression was intermittent heart block seen. This study suggests that in Purkinje fibers, TRPM4 channels may account for sodium background current (I

Indexed as

Electrophysiological PhenomenaGene Expression RegulationAction PotentialsAnimalsDogsMyocytes, CardiacPurkinje FibersSodiumTRPM Cation ChannelsUp-RegulationSodiumTRPM Cation Channels

Identifiers

PMID30598284
PMCPMC6372197
OpenAlexW2905164719

What OpenQuestion 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 OpenQuestion graph.