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Cardiac forces regulate zebrafish heart valve delamination by modulating Nfat signaling. | LitMetric

AI Article Synopsis

  • Most congenital heart valve defects are believed to arise after the endothelial-mesenchymal transition (EndoMT) stage in valve development, but the role of mechanical forces is not well understood.
  • Researchers used zebrafish to study how the superior atrioventricular canal (AVC) transforms into valve leaflets through processes like mesenchymal-endothelial transition (MEndoT) and tissue sheet delamination.
  • Mechanical, chemical, and genetic alterations showed that mechanical forces play a crucial role in regulating valve delamination, impacting heart function and involving the modulation of Nfatc activity.

Article Abstract

In the clinic, most cases of congenital heart valve defects are thought to arise through errors that occur after the endothelial-mesenchymal transition (EndoMT) stage of valve development. Although mechanical forces caused by heartbeat are essential modulators of cardiovascular development, their role in these later developmental events is poorly understood. To address this question, we used the zebrafish superior atrioventricular valve (AV) as a model. We found that cellularized cushions of the superior atrioventricular canal (AVC) morph into valve leaflets via mesenchymal-endothelial transition (MEndoT) and tissue sheet delamination. Defects in delamination result in thickened, hyperplastic valves, and reduced heart function. Mechanical, chemical, and genetic perturbation of cardiac forces showed that mechanical stimuli are important regulators of valve delamination. Mechanistically, we show that forces modulate Nfatc activity to control delamination. Together, our results establish the cellular and molecular signature of cardiac valve delamination in vivo and demonstrate the continuous regulatory role of mechanical forces and blood flow during valve formation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8794269PMC
http://dx.doi.org/10.1371/journal.pbio.3001505DOI Listing

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