ArticlebioRxiv : the preprint server for biology2024
Identification of novel buffering mechanisms in aortic arch artery development and congenital heart disease.
Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors at 2 institutions in 1 country.
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Abstract
Rationale: The resiliency of embryonic development to genetic and environmental perturbations has been long appreciated; however, little is known about the mechanisms underlying the robustness of developmental processes. Aberrations resulting in neonatal lethality are exemplified by congenital heart disease (CHD) arising from defective morphogenesis of pharyngeal arch arteries (PAA) and their derivatives. Objective: To uncover mechanisms underlying the robustness of PAA morphogenesis. Methods and Results: The second heart field (SHF) gives rise to the PAA endothelium. Here, we show that the number of SHF-derived ECs is regulated by Conclusions: Our studies uncover a novel buffering mechanism underlying the resiliency of PAA development and remodeling. Nonstandard Abbreviations and Acronyms in Alphabetical Order: CHD - congenital heart disease; ECs - endothelial cells; IAA-B - interrupted aortic arch type B; PAA - pharyngeal arch arteries; RERSA - retro-esophageal right subclavian artery; SHF - second heart field; VEGFR2 - Vascular endothelial growth factor receptor 2.
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