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Lookup NU author(s): Dr Lorraine Eley, Dr Rachel Richardson, Ahlam Alqahtani, Dr Bill Chaudhry, Professor Deborah HendersonORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2024. Published by The Company of Biologists Ltd. eNOS (NOS3) is the enzyme that generates nitric oxide, a signalling molecule and regulator of vascular tone. Loss of eNOS function is associated with increased susceptibility to atherosclerosis, hypertension, thrombosis and stroke. Aortopathy and cardiac hypertrophy have also been found in eNOS null mice, but their aetiology is unclear. We evaluated eNOS nulls before and around birth for cardiac defects, revealing severe abnormalities in the ventricular myocardium and pharyngeal arch arteries. Moreover, in the aortic arch, there were fewer baroreceptors, which sense changes in blood pressure. Adult eNOS null survivors showed evidence of cardiac hypertrophy, aortopathy and cartilaginous metaplasia in the periductal region of the aortic arch. Notch1 and neuregulin were dysregulated in the forming pharyngeal arch arteries and ventricles, suggesting that these pathways may be relevant to the defects observed. Dysregulation of eNOS leads to embryonic and perinatal death, suggesting mutations in eNOS are candidates for causing congenital heart defects in humans. Surviving eNOS mutants have a deficiency of baroreceptors that likely contributes to high blood pressure and may have relevance to human patients who suffer from hypertension associated with aortic arch abnormalities.
Author(s): Eley L, Richardson RV, Alqahtani A, Chaudhry B, Henderson DJ
Publication type: Article
Publication status: Published
Journal: Disease Models & Mechanisms
Year: 2024
Volume: 17
Issue: 1
Online publication date: 22/01/2024
Acceptance date: 12/12/2023
Date deposited: 07/02/2024
ISSN (print): 1754-8403
ISSN (electronic): 1754-8411
Publisher: The Company of Biologists
URL: https://doi.org/10.1242/dmm.050265
DOI: 10.1242/dmm.050265
Data Access Statement: All relevant data can be found within the article and its supplementary information.
PubMed id: 38111957
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