Evidence map›Paper›PMID 41954126›Full record

ArticleEpilepsia2026

Cardiac remodeling and arrhythmia in a mouse model of Depdc5 haploinsufficiency.

Roberto Ramos-Mondragon, Shuyun Wang, Qinghua Liu, Chunling Chen, Alexander M Greiner, Abigail M Marx, Maya Shih, Jack M Parent, Barry London, Lori L Isom

Abstract read
In one paragraph

Article in Epilepsia, 2026. 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

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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. A Change of Heart forEpilepsy currents · 2026
    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

10 authors.

Roberto Ramos-MondragonDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Shuyun WangDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Qinghua LiuDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Chunling ChenDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Alexander M GreinerDepartment of Internal Medicine-Division of Cardiovascular Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
Abigail M MarxDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Maya ShihDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Jack M ParentDepartment of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Barry LondonDepartment of Internal Medicine-Division of Cardiovascular Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
Lori L IsomDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan, USA.ORCID https://orcid.org/0000-0002-9479-6729

Funding

Cardiac Mechanisms of Sudden Unexpected Death in EpilepsyR01HL149363 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ISOM, LORI L., PARENT, JACK M · 2020 to 2023
$2.8M
Gerber Foundation N026586NHLBI NIH HHS HL149363NHLBI NIH HHS R01 HL149363Vivian L. Cotton Epilepsy Research Fund
6 · The paper itself

Abstract

objectiveSome ion channel genes linked to developmental and epileptic encephalopathy (DEE) are also linked to cardiac arrhythmia, leading to the hypothesis that predisposition to cardiac arrhythmias may contribute to the complex disease presentation of DEE and possibly to the mechanism of sudden unexpected death in epilepsy. However, channelopathies represent only ~25% of the genetic epilepsies. The remainder arise from variants in non-ion-channel genes, moving the disorder beyond channelopathies. Despite evidence that some non-ion-channel variants are linked to sudden cardiac death, we have little information on whether non-ion-channel DEE variants can also result in cardiac phenotypes.

methodsHere, we investigated the DEE gene, DEPDC5, which is expressed in both brain and heart. We studied the cardiac phenotype of a Depdc5 haploinsufficient mouse model that genetically mimics DEPDC5 patients.

resultsDepdc5 SIGNIFICANCE: These data strengthen the hypothesis that cardiac arrhythmias may contribute to the complex presentation of DEE and expand our previous work showing cardiac arrhythmia in multiple mouse and human channelopathy models to include a model of a non-ion-channel variant. Although this work may have implications for DEPDC5 patients, critical differences between mouse and human cardiac physiology complicate the translation of mouse data to human disease. Essential next steps must include investigation of Depdc5 function in higher vertebrate models that more accurately mimic human physiology, as well as longitudinal patient natural history studies that monitor cardiovascular health, to test the hypothesis that DEE variants resulting in DEPDC5 haploinsufficiency may predispose patients to cardiac arrhythmias.

Indexed as

Arrhythmias, CardiacGTPase-Activating ProteinsHaploinsufficiencyVentricular RemodelingAction PotentialsAnimalsDisease Models, AnimalMaleMiceMyocytes, CardiacGTPase-Activating Proteinscardiac arrhythmiadevelopmental and epileptic encephalopathymouse model

Identifiers

PMID41954126
PMCPMC13360907

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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.