Evidence map›Paper›PMID 31468004›Full record

ArticleJACC. Basic to translational science2019

Extracellular Matrix From Hypertrophic Myocardium Provokes Impaired Twitch Dynamics in Healthy Cardiomyocytes.

Lorenzo R Sewanan, Jonas Schwan, Jonathan Kluger, Jinkyu Park, Daniel L Jacoby, Yibing Qyang, Stuart G Campbell

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.9field-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

54 citing papers in PubMed, 72 citations in OpenAlex.

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  7. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
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  9. HeterozygousJournal of applied physiology (Bethesda, Md. : 1985) · 2025
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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.

Lorenzo R SewananDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut.
Jonas SchwanDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut.
Jonathan KlugerDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut.
Jinkyu ParkYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut.
Daniel L JacobyYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut.
Yibing QyangYale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut.
Stuart G CampbellDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut.
Yale University · USYale Cancer Center · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Revealing Pathomechanisms of Mutant TPM1 Through a Hybrid Computational-Experimental ApproachR01HL136590 · NHLBI · YALE UNIVERSITY · PI STUART G CAMPBELL, William J Lehman · 2017 to 2026
$5.6M
Biomechanical Signaling in Human Familial Hypertrophic CardiomyopathyR01HL131940 · NHLBI · YALE UNIVERSITY · PI QYANG, YIBING · 2016 to 2019
$1.7M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL131940NHLBI NIH HHS R01 HL136590NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is often caused by single sarcomeric gene mutations that affect muscle contraction. Pharmacological correction of mutation effects prevents but does not reverse disease in mouse models. Suspecting that diseased extracellular matrix is to blame, we obtained myocardium from a miniature swine model of HCM, decellularized thin slices of the tissue, and re-seeded them with healthy human induced pluripotent stem cell-derived cardiomyocytes. Compared with cardiomyocytes grown on healthy extracellular matrix, those grown on the diseased matrix exhibited prolonged contractions and poor relaxation. This outcome suggests that extracellular matrix abnormalities must be addressed in therapies targeting established HCM.

Indexed as

cDNA, complementary deoxyribonucleic acidCM, cardiomyocytediastolic dysfunctionECM, extracellular matrixEHT, engineered heart tissueengineered heart tissuefibrosisHCM, hypertrophic cardiomyopathyH&E, hematoxylin and eosinhypertrophic cardiomyopathyiPSC-derived cardiomyocyteiPSC, induced pluripotent stem cellMTR, Masson trichromeMUT, minipig carrying MYH7 R403Q mutationMYH7 mutationRT50, time from peak tension to 50% relaxationSR, Sirius redTTP, time to peak tensionWT, wild-type

Identifiers

PMID31468004
PMCPMC6712054
OpenAlexW2962756549

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.