ROLE OF ENDOTHELIAL NITRIC OXIDE SYNTHASE (ENOS) IN FETAL HEART DEVELOPMENT AND ITS IMPLICATIONS ON SEPTAL DEFECTS
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Keywords
Fetal heart development, eNOS mutant, Cardiomyocyte proliferation, Paracrine signaling.#
Abstract
Endothelial nitric oxide synthase is crucial for the formation of the circulatory system during cardiomyogenesis and for maintaining its homeostasis (eNOS). This enzyme synthesizes nitric oxide and it is expressed in the cells of endothelium, an essential signaling molecule involved in several physiological processes. Throughout the development of the embryonic heart, many key processes that influence cardiac morphogenesis and function include angiogenesis, vasculogenesis, and cardiomyocyte proliferation. The regulation of eNOS-mediated nitric oxide generation is critical for the growth of heart chambers and septation in developing hearts. Conditions such as septal defects of ventricles, atrium, and other congenital heart issues can result from disruption with eNOS function. In order to treat symptoms and avoid consequences from these anomalies, which could harm heart function, surgical operations are frequently required. Understanding how eNOS controls activities throughout the development of the embryonic heart is essential to understanding the etiology of congenital cardiac disorders, especially those involving septal abnormalities. There is possibility of improved outcomes for those with these conditions by focusing on medicines that aim to mitigate the consequences of abnormalities through genes in the eNOS pathway. Therefore, this review focuses on the foundational to current significance of the role of eNOS in the formation of the fetal heart and its impacts on congenital cardiac abnormalities that result from eNOS and its signaling pathways being impaired. (www.actabiomedica.it)
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