Evidence map›Paper›PMID 35762211›Full record

ArticleeLife2022

Eric N Jimenez-Vazquez, Michael Arad, Álvaro Macías, Maria L Vera-Pedrosa, Francisco Miguel Cruz, Lilian K Gutierrez, Ashley J Cuttitta, André Monteiro da Rocha, Todd J Herron, Daniela Ponce-Balbuena and 4 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2025
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  15. Watching Ion Channels on the Move.Function (Oxford, England) · 2023
    Article
  16. Article
  17. 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

14 authors at 4 institutions in 3 countries.

Eric N Jimenez-VazquezDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.ORCID https://orcid.org/0000-0001-5134-491X
Michael AradLeviev Heart Center, Sheba Medical Center, Tel Hashomer, and Tel Aviv University, Tel Aviv, Israel.
Álvaro MacíasCentro Nacional de Investigaciones Cardiovasculares (CNIC) Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.ORCID https://orcid.org/0000-0002-9952-6947
Maria L Vera-PedrosaCentro Nacional de Investigaciones Cardiovasculares (CNIC) Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.ORCID https://orcid.org/0000-0001-9861-7284
Francisco Miguel CruzCentro Nacional de Investigaciones Cardiovasculares (CNIC) Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.ORCID https://orcid.org/0000-0001-5330-8613
Lilian K GutierrezCentro Nacional de Investigaciones Cardiovasculares (CNIC) Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.ORCID https://orcid.org/0000-0003-1476-723X
Ashley J CuttittaDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, United States.ORCID https://orcid.org/0000-0002-2400-4087
André Monteiro da RochaDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.ORCID https://orcid.org/0000-0003-3324-3773
Todd J HerronDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.
Daniela Ponce-BalbuenaDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.ORCID https://orcid.org/0000-0002-7413-5325
Guadalupe Guerrero-SernaDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.ORCID https://orcid.org/0000-0001-9130-1850
Ofer BinahDepartment of Physiology, Biophysics and Systems Biology, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.
Daniel E MicheleDepartment of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, United States.ORCID https://orcid.org/0000-0003-4393-4551
José JalifeDepartment of Internal Medicine and Molecular and Integrative Physiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, United States.ORCID https://orcid.org/0000-0003-0080-3500
University of Michigan · USCentro de Investigación en Red en Enfermedades Cardiovasculares · ESTechnion – Israel Institute of Technology · ILTel Aviv University · IL

Funding

Intermolecular Interactions of NaV1.5 and Kir2.1 In Ion Channel DiseasesR01HL122352 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERENFELD, OMER · 2015 to 2018
$1.9M
Mechanosignaling Functions of the Dystrophin Glycoprotein Complex in Muscular DystrophyR01AR068428 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MICHELE, DANIEL E · 2016 to 2020
$1.7M
NHLBI NIH HHS R01 HL122352NIAMS NIH HHS R01 AR068428
6 · The paper itself

Abstract

Background: Patients with cardiomyopathy of Duchenne Muscular Dystrophy (DMD) are at risk of developing life-threatening arrhythmias, but the mechanisms are unknown. We aimed to determine the role of ion channels controlling cardiac excitability in the mechanisms of arrhythmias in DMD patients. Methods: To test whether dystrophin mutations lead to defective cardiac Na Results: Two patients had abnormal ECGs with frequent runs of ventricular tachycardia. iPSC-CMs from all DMD patients showed abnormal action potential profiles, slowed conduction velocities, and reduced sodium (I Conclusions: We provide the first demonstration that iPSC-CMs reprogrammed from skin fibroblasts of DMD patients with cardiomyopathy have a dysfunction of the Na Funding: Supported by National Institutes of Health R01 HL122352 grant; 'la Caixa' Banking Foundation (HR18-00304); Fundación La Marató TV3:

Indexed as

Calcium-Binding ProteinsCardiomyopathiesInduced Pluripotent Stem CellsMembrane ProteinsMuscle ProteinsMuscular Dystrophy, DuchennePotassium Channels, Inwardly RectifyingAction PotentialsArrhythmias, CardiacDystrophinFemaleHumansMaleMyocytes, CardiacCalcium-Binding ProteinsDystrophinMembrane ProteinsMuscle ProteinsPotassium Channels, Inwardly Rectifyingsyntrophin alpha1cell biologydystrophin-associated protein complexhumanmedicineNaV1.5–Kir2.1 channelosomepatient-specific hiPSC-CMsudden cardiac death

Identifiers

PMID35762211
PMCPMC9239678
OpenAlexW4283701283

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.