The Impact of Mechanical Forces in Heart Morphogenesis
Abstract
C ongenital heart disease (CHD) is the most common birth defect in humans and results from deficient cardiac development, a complex process that is not completely understood.The heart starts to function before its morphogenesis is complete and the increasing needs of the growing embryo for oxygen and nutrients demand a proportional increase in the performance of the organ.We review recent findings supporting the hypothesis that the activity of the developing heart influences its morphogenesis and that internal or external factors, which significantly modify its functional capability, can in turn, induce anatomic cardiac defects.We propose that a role for early cardiac contraction in heart development is supported by recent experimental evidence and that the Notch pathway acts as a key transducer between hemodynamic stimuli and cardiogenesis.
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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.”
From Cell diversity and plasticity during atrioventricular heart valve EMTs (2023) · cites this paper as [11]
The Conclusions and Figure 2 describe blood-flow-related shear stress increasing Notch activity in endocardial cushion cells, some of which undergo EMT. But The Notch Connection places the start of mouse cushion EMT at E9.5, not E9.0. Its BMP10 discussion concerns trabecular cardiomyocyte proliferation, not myocardial BMP signals inducing cushion EndMT; no page numbers are available in our copy. (LLM, conf=0.89)
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- Authors
- Granados-Riveron, J. T., & Brook, J. D.
- Affiliations
- University of Nottingham (GB)
- Venue
- Circulation: Cardiovascular Genetics
- Published
- 2012-02
- Volume
- 5
- Issue
- 1
- Pages
- 132-142
- ISSN
- 1942-325X (ISSN-L)
- 1942-3268
- OpenAlex
- W2072622848
- Cited by
- 90
- References
- 105
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 15 · 2015: 7 · 2014: 12 · 2013: 4 · 2012: 1
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Cardiovascular Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (RG/07/010, RG/07/010/23676)
- Consejo Nacional de Ciencia y Tecnología
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- mechanical forces, cardiac morphogenesis, congenital heart disease, heart development, Notch signaling, cardiac defects
- MeSH terms
- Animals, Heart, Heart Defects, Congenital, Hemodynamics, Humans, Models, Biological, Morphogenesis, Myocardial Contraction, Signal Transduction, Myosin Heavy Chains, Cardiac Myosins, Shear Strength, Receptors, Notch
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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