Endothelial intric oxide synthase in the cardiomyocyte : modulatory roles on contractility and cell biology
(2005)
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- Authors
- Supervisors
- Balligand, Jean-Luc
- Abstract
- Selective myocyte eNOS overexpression improves the sympathovagal balance of the heart and protects it against excessive beta-adrenegic stimulation, in part through potentiation of vagal inhibition of cardiac contraction and prevention of ectopic contractions. Benefit of eNOS overexpression can further be extended on cardiac stem cells, with a favorable role of eNOS on their transdifferentiation and possibly on their survival through an anti-apopotic effect. Finally, cardioprotective drugs such as statins and insulin precisely increase myocyte eNOS expression. This observation links well-known unexplained pleiotropic effects to a potential powerful mechanism, i.e. an increase of endogenous myocyte eNOS expression and activity. Myocyte eNOS can be considered as an "endogenous b-blocker" for the heart. It is also a key protein in the survival response of the cardiomyocyte, working in conjunction with others (e.g. PKB, insulin ), even able to promote cardiac regeneration. Finally, myocyte eNOS is a common effector of many cardioprotective drugs or even assist device, and its preservation in patients could prevent their evolution to cardiac decompensation.
- Affiliations
Citations
Massion, P. (2005). Endothelial intric oxide synthase in the cardiomyocyte : modulatory roles on contractility and cell biology. https://hdl.handle.net/2078.5/129678