Evidence map›Paper›PMID 25209314›Full record

ArticleCardiovascular research2014

Study familial hypertrophic cardiomyopathy using patient-specific induced pluripotent stem cells.

Lu Han, Yang Li, Jason Tchao, Aaron D Kaplan, Bo Lin, You Li, Jocelyn Mich-Basso, Agnieszka Lis, Narmeen Hassan, Barry London and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 2 pooled it
11.4field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.

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  19. Incomplete-penetrant hypertrophic cardiomyopathyProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article

57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Lu HanDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Yang LiDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Jason TchaoDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Aaron D KaplanCenter for Cellular and Systems Electrophysiology, Department of Physiology and Biophysics, SUNY, Buffalo, NY 14214, USA.
Bo LinDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
You LiDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Jocelyn Mich-BassoDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Agnieszka LisCenter for Cellular and Systems Electrophysiology, Department of Physiology and Biophysics, SUNY, Buffalo, NY 14214, USA.
Narmeen HassanDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Barry LondonDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Glenna C L BettDepartment of Obstetrics and Gynecology, SUNY, Buffalo, NY 14214, USA.
Kimimasa TobitaDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA.
Randall L RasmussonCenter for Cellular and Systems Electrophysiology, Department of Physiology and Biophysics, SUNY, Buffalo, NY 14214, USA.
Lei YangDepartment of Developmental Biology, University of Pittsburgh School of Medicine, 8117 Rangos Research Center, 530 45th Street, Pittsburgh, PA 15201, USA lyang@pitt.edu.
University of Pittsburgh · USUniversity at Buffalo, State University of New York · USUniversity of Iowa · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Markov Models of Potassium Channel GatingR01HL062465 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI RASMUSSON, RANDALL L. · 1998 to 2012
$3.5M
Sex Differences in Molecular Heterogeneity of Cardiac RepolarizationR21HL093631 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI BETT, GLENNA C L · 2011 to 2012
$429k
Three-Dimensional Cardiac Gel Bioreactor for Functioning Cardiomyocyte Induction R21HL094402 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TOBITA, KIMIMASA · 2009 to 2010
$410k
NCATS NIH HHS UL1TR000005NHLBI NIH HHS HL062465NHLBI NIH HHS HL093631NHLBI NIH HHS R21 HL094402NHLBI NIH HHS T32-HL76124
6 · The paper itself

Abstract

aimsFamilial hypertrophic cardiomyopathy (HCM) is one the most common heart disorders, with gene mutations in the cardiac sarcomere. Studying HCM with patient-specific induced pluripotent stem-cell (iPSC)-derived cardiomyocytes (CMs) would benefit the understanding of HCM mechanism, as well as the development of personalized therapeutic strategies. METHODS AND

resultsTo investigate the molecular mechanism underlying the abnormal CM functions in HCM, we derived iPSCs from an HCM patient with a single missense mutation (Arginine442Glycine) in the MYH7 gene. CMs were next enriched from HCM and healthy iPSCs, followed with whole transcriptome sequencing and pathway enrichment analysis. A widespread increase of genes responsible for 'Cell Proliferation' was observed in HCM iPSC-CMs when compared with control iPSC-CMs. Additionally, HCM iPSC-CMs exhibited disorganized sarcomeres and electrophysiological irregularities. Furthermore, disease phenotypes of HCM iPSC-CMs were attenuated with pharmaceutical treatments.

conclusionOverall, this study explored the possible patient-specific and mutation-specific disease mechanism of HCM, and demonstrates the potential of using HCM iPSC-CMs for future development of therapeutic strategies. Additionally, the whole methodology established in this study could be utilized to study mechanisms of other human-inherited heart diseases.

Indexed as

Action PotentialsAdultAnimalsCalcium SignalingCardiac MyosinsCardiomyopathy, Hypertrophic, FamilialCase-Control StudiesCell ProliferationCells, CulturedCell SeparationCellular ReprogrammingCellular Reprogramming TechniquesFemaleGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksCardiac MyosinsMYH7 protein, humanMyosin Heavy ChainsCardiomyocyteHeartHypertrophic cardiomyopathyInduced pluripotent stem cells

Identifiers

PMID25209314
PMCPMC4217687
OpenAlexW2149847832

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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.