Evidence map›Paper›PMID 39616198›Full record

ArticleScientific reports2024

A novel computational model of swine ventricular myocyte reveals new insights into disease mechanisms and therapeutic approaches in Timothy Syndrome.

Alessandro Trancuccio, Carmen Tarifa, Rossana Bongianino, Silvia G Priori, Demetrio J Santiago

Abstract read
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In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

5 authors.

Alessandro TrancuccioMolecular Cardiology Unit, IRCCS Istituti Clinici Scientifici Maugeri, Pavia, Italy.
Carmen TarifaNovel Arrhythmogenic Mechanisms Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Rossana BongianinoMolecular Cardiology Unit, IRCCS Istituti Clinici Scientifici Maugeri, Pavia, Italy.
Silvia G PrioriMolecular Cardiology Unit, IRCCS Istituti Clinici Scientifici Maugeri, Pavia, Italy.
Demetrio J SantiagoNovel Arrhythmogenic Mechanisms Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. demetriojulian.santiago@cnic.es.

Funding

European Research Council ERC-ADG-2014-ID:669387Fondazione Telethon GMR22T1100
6 · The paper itself

Abstract

Timothy syndrome type 1 (TS1), a malignant variant of Long QT Syndrome, is caused by L-type Ca2+ Channel (LTCC) inactivation defects secondary to the p.Gly406Arg mutation in the CACNA1C gene. Leveraging on the experimental in vitro data from our TS1 knock-in swine model and their wild-type (WT) littermates, we first developed a mathematical model of WT large white swine ventricular cardiomyocyte electrophysiology that reproduces a wide range of experimental data, including ionic current properties, action potential (AP) dynamics, and

Indexed as

Action PotentialsAutistic DisorderCalcium Channels, L-TypeHeart VentriclesLong QT SyndromeMyocytes, CardiacSyndactylyAnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Computer SimulationDisease Models, AnimalHumansModels, CardiovascularMutationSwineCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeL-type calcium channel alpha(1C)CACNA1CCardiac ElectrophysiologyLong QT SyndromeMathematical ModelingSwine Ventricular Myocyte

Identifiers

PMID39616198
PMCPMC11608236

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Registered trials

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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.