Evidence map›Paper›PMID 35219725›Full record

ArticleJournal of molecular and cellular cardiology2022

Changes in extracellular matrix in failing human non-ischemic and ischemic hearts with mechanical unloading.

Yimu Zhao, Amandine Godier-Furnemont, Noortje A M Bax, Carlijn V C Bouten, Lewis M Brown, Barry Fine, Gordana Vunjak-Novakovic

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

Article in Journal of molecular and cellular cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. 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

7 authors at 2 institutions in 2 countries.

Yimu ZhaoDepartment of Biomedical Engineering, Columbia University, New York 10032, USA.
Amandine Godier-FurnemontDepartment of Biomedical Engineering, Columbia University, New York 10032, USA.
Noortje A M BaxDepartment of Biomedical Engineering, Columbia University, New York 10032, USA; Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands; Center for Care & Cure Technology Eindhoven (C3Te), Eindhoven University, Eindhoven, the Netherlands.
Carlijn V C BoutenDepartment of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands; Institute for Complex Molecular Systems, Eindhoven University of Technology, Eindhoven, the Netherlands.
Lewis M BrownQuantitative Proteomics and Metabolomics Center, Department of Biological Sciences, Columbia University, New York 10027, USA.
Barry FineDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Gordana Vunjak-NovakovicDepartment of Biomedical Engineering, Columbia University, New York 10032, USA; Department of Medicine, Columbia University, New York, NY 10032, USA. Electronic address: gv2131@columbia.edu.
Columbia University · USEindhoven University of Technology · NL

Funding

Tissue Engineering Resource Center: TTDP41EB027062 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Gordana Vunjak-Novakovic · 2019 to 2026
$12.6M
Engineering Vascularized Cardiac MuscleR01HL076485 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Gordana Vunjak-Novakovic · 2005 to 2026
$9.2M
Multi-tissue platform for modeling systemic pathologiesUH3EB025765 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VUNJAK-NOVAKOVIC, GORDANA · 2019 to 2021
$4.0M
The STK25 Signaling Pathway in Human Cardiac CellsK08HL140201 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FINE, BARRY M. · 2018 to 2022
$831k
NHLBI NIH HHS K08 HL140201NHLBI NIH HHS R01 HL076485NIBIB NIH HHS P41 EB027062NIBIB NIH HHS UH3 EB025765
6 · The paper itself

Abstract

Ischemic and non-ischemic cardiomyopathies have distinct etiologies and underlying disease mechanisms, which require in-depth investigation for improved therapeutic interventions. The goal of this study was to use clinically obtained myocardium from healthy and heart failure patients, and characterize the changes in extracellular matrix (ECM) in ischemic and non-ischemic failing hearts, with and without mechanical unloading. Using tissue engineering methodologies, we also investigated how diseased human ECM, in the absence of systemic factors, can influence cardiomyocyte function. Heart tissues from heart failure patients with ischemic and non-ischemic cardiomyopathy were compared to explore differential disease phenotypes and reverse remodeling potential of left ventricular assisted device (LVAD) support at transcriptomic, proteomic and structural levels. The collected data demonstrated that the differential ECM compositions recapitulated the disease microenvironment and induced cardiomyocytes to undergo disease-like functional alterations. In addition, our study also revealed molecular profiles of non-ischemic and ischemic heart failure patients and explored the underlying mechanisms of etiology-specific impact on clinical outcome of LVAD support and tendency towards reverse remodeling.

Indexed as

Heart-Assist DevicesHeart FailureExtracellular MatrixHumansMyocardiumProteomicsDisease nichesExtracellular matrixHeart failureIschemic cardiomyopathyLVAD supportNon-ischemic cardiomyopathyProteomics

Identifiers

PMID35219725
PMCPMC9035113
OpenAlexW4213425128

What OpenQuestion holds

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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.