Evidence map›Paper›PMID 31237233›Full record

ArticleeLife2019

Hemodynamic-mediated endocardial signaling controls in vivo myocardial reprogramming.

Manuel Gálvez-Santisteban, Danni Chen, Ruilin Zhang, Ricardo Serrano, Cathleen Nguyen, Long Zhao, Laura Nerb, Evan M Masutani, Julien Vermot, Charles Geoffrey Burns and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 55 citations in OpenAlex.

  1. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
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  3. BMPR2 affects valve development via ECM-receptor interaction in zebrafish.Frontiers in cell and developmental biology · 2026
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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

13 authors at 4 institutions in 3 countries.

Manuel Gálvez-Santisteban *Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, United States.ORCID 0000-0003-3804-1513
Danni Chen *Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, United States.
Ruilin Zhang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Ricardo SerranoMechanical and Aerospace Engineering Department, University of California, San Diego, La Jolla, United States.
Cathleen NguyenMechanical and Aerospace Engineering Department, University of California, San Diego, La Jolla, United States.
Long ZhaoDepartment of Medicine, Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, United States.
Laura NerbDepartment of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, United States.
Evan M MasutaniDepartment of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, United States.
Julien VermotInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, UMR7104, INSERM U964, Université de Strasbourg, Illkirch, France.ORCID 0000-0002-8924-732X
Charles Geoffrey BurnsDepartment of Medicine, Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, United States.ORCID 0000-0002-5812-6621
Caroline E BurnsDepartment of Medicine, Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, United States.
Juan C Del ÁlamoMechanical and Aerospace Engineering Department, University of California, San Diego, La Jolla, United States.
Neil C ChiDepartment of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, United States.ORCID 0000-0003-2324-3796
University of California San Diego · USHarvard University · USFudan University · CNInserm · FR

Funding

Change of InstitutionR35HL135831 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BURNS, CAROLINE E · 2017 to 2023
$4.2M
Modeling thoracic aortic aneurysm in zebrafishR01HL139806 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BURNS, C. GEOFFREY · 2018 to 2021
$1.7M
Deciphering the role of Notch signaling in zebrafish heart regenerationR01HL127067 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BURNS, C. GEOFFREY, BURNS, CAROLINE E · 2015 to 2018
$1.7M
Hemodynamic Flow-Mediated Myocardial Reprogramming Impacts Cardiac DevelopmentR01HD092216 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C · 2018 to 2022
$1.6M
Regulatory Mechanisms of Myocardial Reprogramming in ZebrafishR01HL132298 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C · 2017 to 2020
$1.6M
Regulatory Mechanisms of Cardiomyocyte Lineage SpecificationR01HL139709 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C · 2018 to 2021
$1.2M
NHLBI NIH HHS R01 HL127067NHLBI NIH HHS R01 HL132298NHLBI NIH HHS R01 HL139709NHLBI NIH HHS R01 HL139806NHLBI NIH HHS R35 HL135831NICHD NIH HHS R01 HD092216NIH HHS R01HL127067
6 · The paper itself

Abstract

Lower vertebrate and neonatal mammalian hearts exhibit the remarkable capacity to regenerate through the reprogramming of pre-existing cardiomyocytes. However, how cardiac injury initiates signaling pathways controlling this regenerative reprogramming remains to be defined. Here, we utilize in vivo biophysical and genetic fate mapping zebrafish studies to reveal that altered hemodynamic forces due to cardiac injury activate a sequential endocardial-myocardial signaling cascade to direct cardiomyocyte reprogramming and heart regeneration. Specifically, these altered forces are sensed by the endocardium through the mechanosensitive channel Trpv4 to control Klf2a transcription factor expression. Consequently, Klf2a then activates endocardial Notch signaling which results in the non-cell autonomous initiation of myocardial Erbb2 and BMP signaling to promote cardiomyocyte reprogramming and heart regeneration. Overall, these findings not only reveal how the heart senses and adaptively responds to environmental changes due to cardiac injury, but also provide insight into how flow-mediated mechanisms may regulate cardiomyocyte reprogramming and heart regeneration.

Indexed as

HemodynamicsMechanotransduction, CellularRegenerationAnimalsEndocardiumHeart InjuriesKruppel-Like Transcription FactorsMyocytes, CardiacReceptors, NotchTRPV Cation ChannelsZebrafishZebrafish ProteinsKlf2a protein, zebrafishKruppel-Like Transcription FactorsReceptors, NotchTRPV4 protein, zebrafishTRPV Cation ChannelsZebrafish Proteinsdevelopmental biologygeneticshearthemodynamicsregenerationreprogrammingzebrafish

Identifiers

PMID31237233
PMCPMC6592682
OpenAlexW2952747634

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.