Evidence map›Paper›PMID 26044252›Full record

ReviewCirculation research2015

Finding the rhythm of sudden cardiac death: new opportunities using induced pluripotent stem cell-derived cardiomyocytes.

Karim Sallam, Yingxin Li, Philip T Sager, Steven R Houser, Joseph C Wu

Abstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

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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 at 1 institution in 1 country.

Karim SallamFrom the Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute (K.S., Y.L., P.T.S., J.C.W.), Institute of Stem Cell Biology and Regenerative Medicine (K.S., Y.L., J.C.W.), Stanford University School of Medicine, CA; and Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (S.R.H.).
Yingxin LiFrom the Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute (K.S., Y.L., P.T.S., J.C.W.), Institute of Stem Cell Biology and Regenerative Medicine (K.S., Y.L., J.C.W.), Stanford University School of Medicine, CA; and Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (S.R.H.).
Philip T SagerFrom the Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute (K.S., Y.L., P.T.S., J.C.W.), Institute of Stem Cell Biology and Regenerative Medicine (K.S., Y.L., J.C.W.), Stanford University School of Medicine, CA; and Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (S.R.H.).
Steven R HouserFrom the Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute (K.S., Y.L., P.T.S., J.C.W.), Institute of Stem Cell Biology and Regenerative Medicine (K.S., Y.L., J.C.W.), Stanford University School of Medicine, CA; and Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (S.R.H.). joewu@stanford.edu srhouser@temple.edu.
Joseph C WuFrom the Division of Cardiology, Department of Medicine, Stanford Cardiovascular Institute (K.S., Y.L., P.T.S., J.C.W.), Institute of Stem Cell Biology and Regenerative Medicine (K.S., Y.L., J.C.W.), Stanford University School of Medicine, CA; and Cardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (S.R.H.). joewu@stanford.edu srhouser@temple.edu.
Cardiovascular Institute of the South · US

Funding

PKC alpha as a translational target in Heart FailureP01HL108806 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RABINOWITZ, JOSEPH E · 2012 to 2016
$11.3M
Biorepository of Human iPSCs for Studying Dilated and Hypertrophic CardiomyopathyR24HL117756 · NHLBI · STANFORD UNIVERSITY · PI BUSTAMANTE, CARLOS DANIEL, SNYDER, MICHAEL P. · 2014 to 2018
$8.8M
Human Induced Pluripotent Stem Cells for Cardiovascular Disease ModelingR01HL113006 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2012 to 2025
$6.8M
Calcium and Cardiac Regeneration after Myocardial InfarctionR01HL033921 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI HOUSER, STEVEN R · 1985 to 2017
$5.6M
Genome Editing of Human iPSCs to Study Inherited Hypertrophic CardiomyopathyR01HL126527 · NHLBI · STANFORD UNIVERSITY · PI QI, LEI STANLEY, WU, JOSEPH C. · 2015 to 2022
$5.4M
Training in Myocardial Biology at Stanford (TIMBS)T32HL094274 · NHLBI · STANFORD UNIVERSITY · PI Euan A Ashley, Daniel Bernstein · 2010 to 2026
$5.0M
Modeling Susceptibility to Chemotherapy-Induced Cardiotoxicity Using Human iPSCsR01HL123968 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, WU, JOSEPH C. · 2014 to 2021
$4.8M
NHLBI NIH HHS P01 HL108806NHLBI NIH HHS R01 HL033921NHLBI NIH HHS R01 HL113006NHLBI NIH HHS R01 HL123968NHLBI NIH HHS R01 HL126527NHLBI NIH HHS R24 HL117756NHLBI NIH HHS T32 HL094274PHS HHS P01 108806
6 · The paper itself

Abstract

Sudden cardiac death is a common cause of death in patients with structural heart disease, genetic mutations, or acquired disorders affecting cardiac ion channels. A wide range of platforms exist to model and study disorders associated with sudden cardiac death. Human clinical studies are cumbersome and are thwarted by the extent of investigation that can be performed on human subjects. Animal models are limited by their degree of homology to human cardiac electrophysiology, including ion channel expression. Most commonly used cellular models are cellular transfection models, which are able to mimic the expression of a single-ion channel offering incomplete insight into changes of the action potential profile. Induced pluripotent stem cell-derived cardiomyocytes resemble, but are not identical, adult human cardiomyocytes and provide a new platform for studying arrhythmic disorders leading to sudden cardiac death. A variety of platforms exist to phenotype cellular models, including conventional and automated patch clamp, multielectrode array, and computational modeling. Induced pluripotent stem cell-derived cardiomyocytes have been used to study long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy, and other hereditary cardiac disorders. Although induced pluripotent stem cell-derived cardiomyocytes are distinct from adult cardiomyocytes, they provide a robust platform to advance the science and clinical care of sudden cardiac death.

Indexed as

Death, Sudden, CardiacAnimalsCardiovascular AgentsCell DifferentiationCells, CulturedClinical Trials as TopicComputer SimulationDisease Models, AnimalDrug Evaluation, PreclinicalElectrophysiologyForecastingHeart DiseasesHumansInduced Pluripotent Stem CellsIon ChannelsLong QT SyndromeCardiovascular AgentsIon Channelscardiovascular diseasesdeath, sudden, cardiacdrug discoveryinduced pluripotent stem cells

Identifiers

PMID26044252
PMCPMC4676576
OpenAlexW1933404492

What OpenQuestion holds

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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.