ArticleMathematical biosciences2016
A mathematical model of endothelial nitric oxide synthase activation with time delay exhibiting Hopf bifurcation and oscillations.
Article in Mathematical biosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- Endothelial dysfunction due to selective insulin resistance in vascular endothelium: insights from mechanistic modeling.American journal of physiology. Endocrinology and metabolism · 2020 · on this mapArticle
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Abstract
Nitric oxide (NO) is a gaseous compound that serves as a signaling molecule in cellular interactions. In the vasculature, NO is synthesized from endogenous agents by endothelial nitric oxide synthase (eNOS) where it plays key roles in several functions related to homeostasis, adaptation, and development. Recent experimental studies have revealed cycles of increasing and decreasing NO production when eNOS is stimulated by factors such as glucose or insulin. We offer a mathematical model of a generic amino acid receptor site on eNOS wherein this species is subject to activation/deactivation by a pair of interactive kinase and phosphatase species. The enzyme kinetic model is presented as a system of ordinary differential equations including time delay to allow for various intermediate, unspecified complexes. We show that under conditions on the model parameters, varying the delay time may give rise to a Hopf bifurcation. Properties of the bifurcating solutions are explored via a center manifold reduction, and a numerical illustration is provided.
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