通过数学建模和计算机分析,揭示高血压与Covid - 19患者炎症反应之间的相互依存关系

Rosario Pacheco-Marin, Carolina Caballero-Cordero, Jorge Arturo Arciniega-González, E. Álvarez-Buylla, Juan Carlos Martínez-García
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引用次数: 0

摘要

我们在此探讨了决定人类血压模式的基于系统的调节机制。这是在高血压与COVID-19疾病呈负相关的背景下进行的。我们对血管紧张素转换酶2 (ACE2)的关键作用特别感兴趣,ACE2是首批确定的使SARS-CoV-2病毒进入细胞的受体之一。考虑到参与血压调节的两个主要系统,即肾素-血管紧张素系统和Kallikrein-Kinin系统,我们遵循自下而上的系统生物学建模方法,以建立典型高血压表型和低血压/正常血压表型基础的基因调控网络的离散布尔模型。这些表型对应于基于公开可用的实验信息建模的调控网络的动态吸引子。我们的模型恢复了观察到的表型,并显示了炎症反应在高血压出现中发挥的关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Uncovering the interdependence between hypertension and the inflammatory response for the patient affected by Covid 19 through mathematical modeling and computer-based analysis
We explore here the systems-based regulatory mechanisms that determine human blood pressure patterns. This in the context of the reported negative association between hypertension and COVID-19 disease. We are particularly interested in the key role that plays angiotensin converting enzyme 2 (ACE2), one of the first identified receptors that enable the entry of the SARS-CoV-2 virus into a cell. Taking into account the two main systems involved in the regulation of blood pressure, that is, the Renin-Angiotensin system and the Kallikrein-Kinin system, we follow a Bottom-Up systems biology modeling approach in order to built the discrete Boolean model of the gene regulatory network that underlies both the typical hypertensive phenotype and the hypotensive/normotensive phenotype. These phenotypes correspond to the dynamic attractors of the regulatory network modeled on the basis of publicly available experimental information. Our model recovers the observed phenotypes and shows the key role played by the inflammatory response in the emergence of hypertension.
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