Evidence map›Paper›PMID 30062212›Full record

ArticleJACC. Basic to translational science2018

Increased Afterload Augments Sunitinib-Induced Cardiotoxicity in an Engineered Cardiac Microtissue Model.

Rachel Truitt, Anbin Mu, Elise A Corbin, Alexia Vite, Jeffrey Brandimarto, Bonnie Ky, Kenneth B Margulies

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Dynamic control of contractile resistance to iPSC-derived micro-heart muscle arrays.Journal of biomedical materials research. Part A · 2024
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  16. Cardio-Oncology: Mechanisms, Drug Combinations, and Reverse Cardio-Oncology.International journal of molecular sciences · 2022
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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

7 authors at 2 institutions in 1 country.

Rachel TruittDepartment of Bioengineering, School of Engineering and Applied Sciences, University of Pennsylvania, Philadelphia, Pennsylvania.
Anbin MuCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Elise A CorbinCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Alexia ViteCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Jeffrey BrandimartoCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Bonnie KyCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kenneth B MarguliesCardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
University of Pennsylvania · USCardiovascular Institute of the South · US

Funding

INSTITUTIONAL CLINICAL AND TRANSLATIONAL SCIENCE AWARDUL1RR024134 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$70.4M
Institutional Clinical and Translational Science AwardUL1TR000003 · NCATS · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2012 to 2015
$38.9M
Training Program in Cardiovascular Biology and MedicineT32HL007843 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI THOMAS P. CAPPOLA, Sharlene M Day · 1996 to 2026
$11.0M
Integrative genomics of human heart failureR01HL105993 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ASHLEY, EUAN A, CAPPOLA, THOMAS P. · 2011 to 2014
$8.9M
Mid Atlantic Heart Failure NetworkU10HL110338 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CAPPOLA, THOMAS P., MARGULIES, KENNETH BER · 2012 to 2018
$2.4M
NCATS NIH HHS UL1 TR000003NCRR NIH HHS UL1 RR024134NHLBI NIH HHS T32 HL007843
6 · The paper itself

Abstract

Sunitinib, a multitargeted oral tyrosine kinase inhibitor, used widely to treat solid tumors, results in hypertension in up to 47% and left ventricular dysfunction in up to 19% of treated individuals. The relative contribution of afterload toward inducing cardiac dysfunction with sunitinib treatment remains unknown. We created a preclinical model of sunitinib cardiotoxicity using engineered microtissues that exhibited cardiomyocyte death, decreases in force generation, and spontaneous beating at clinically relevant doses. Simulated increases in afterload augmented sunitinib cardiotoxicity in both rat and human microtissues, which suggest that antihypertensive therapy may be a strategy to prevent left ventricular dysfunction in patients treated with sunitinib.

Indexed as

2D, 2-dimensional3D, 3-dimensionalafterloadAICAR, 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranosideAMPK, adenosine monophosphate-activated protein kinaseapoptosisATP, adenosine triphosphatecardiotoxicityCCCP, carbonyl cyanide m-chlorophenyl hydrazineCMT, cardiac microtissueDMSO, dimethyl sulfoxideEDTA, ethylenediamine tetraacetic acidHu-iPS-CM, human induced pluripotent stem cell cardiomyocytehuMSC, human mesenchymal stem celliPS-CM, induced pluripotent stem cell-derived cardiomyocyteLV, left ventricleNRVM, neonatal rat ventricular myocytePDMS, polydimethylsiloxaneRPMI, Roswell Park Memorial Institute mediumsunitinibtissue engineeringTMRM, tetramethylrhodaminetoxicologytyrosine kinase inhibitors

Identifiers

PMID30062212
PMCPMC6059907
OpenAlexW2801312657

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.