Cited by 103Congenital heart defects researchCardiac electrophysiology and arrhythmiasDevelopmental Biology and Gene Regulation

Bioelectric signaling and the control of cardiac cell identity in response to mechanical forces

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Fukui, Hajime, Chow, Renee Wei-Yan, Xie, Jing, Foo, Yoke Yin, Yap, Choon Hwai, Minc, Nicolas, Mochizuki, Naoki, Vermot, Julien·2021·Science

Abstract

Making cardiac valves via mechanical forces: Cardiac valves form in response to mechanical forces generated by the beating heart. Fukui et al . studied how patterning signals are generated in response to these forces (see the Perspective by Jain and Epstein). They show that two mechanotransduction pathways act in parallel to instruct cardiac valve progenitors: a well-established transient receptor potential mechanosensation pathway and an extracellular ATP-dependent purinergic receptor pathway that triggers Ca 2+ oscillations and results in nuclear translocation of the protein nuclear factor of activated T cells 1. These two synergistic mechanotransduction pathways generate positional information and control valve formation. The use of multiple pathways may be a general mechanism used by mechanosensitive biological systems to increase the robustness and precision of mechanotransduction. —BAP

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Crossref · 10.1126/science.abc6229

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  • By E9.0, fluid shear stress from blood flow and signals from the myocardium including BMPs induce EndMT in a subset of endocardial cells lining the cushions.

    “By E9.0, fluid shear stress from blood flow and signals from the myocardium, including BMPs, induce an endocardial-to-mesenchymal transition (EndMT) in a subset of endocardial cells lining the cushions9–13.”
  • Piezo1 acts as the major mechanosensor sensing fluid shear stress during EndMT in mouse.

    “suggesting it acts as the major mechanosensor sensing fluid shear stress during EndMT in mouse, as is observed in zebrafish13,49”

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References 55 · Cited by 103

Authors
Fukui, H., Chow, R. W.-Y., Xie, J., Foo, Y. Y., Yap, C. H., Minc, N., Mochizuki, N., & Vermot, J.
Affiliations
  • Centre National de la Recherche Scientifique (FR)
  • Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Centre National de la Recherche Scientifique UMR7104, Institut National de la Santé et de la Recherche Médicale U1258 and Université de Strasbourg, Illkirch, France.
  • National University of Singapore (SG)
  • National Cerebral and Cardiovascular Center Research Institute (JP)
Corresponding author
Vermot, Julien
Venue
Science
Published
2021-10-15
Volume
374
Issue
6565
Pages
351-354
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W3205316755
Cited by
103
References
55
Citations by year
2026: 8 · 2025: 26 · 2024: 31 · 2023: 15 · 2022: 21 · 2021: 2
FWCI
5.41
Type
journal article
Language
en
Open access
Licence
other-oa
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • HAL (submittedVersion, other-oa)
Funders
  • Agence Nationale de la Recherche (ANR-10-IDEX-0002, ANR-18-CE93-0006, ANR-10-LABX-0030, ANR-12-ISV2-0001, ANR-15-CE13-0015)
  • Japan Society for the Promotion of Science (21K06764)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords
mechanotransduction, mechanical forces, TRP channels, purinergic signaling, extracellular ATP, calcium oscillations, positional information, heart development
MeSH terms
Adenosine Triphosphate, Animals, Calcium, Heart Valves, Stress, Mechanical, Zebrafish, Receptors, Purinergic P2, Calcium Signaling, Shear Strength, Endothelial Cells, NFATC Transcription Factors, Electrophysiological Phenomena

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