建立SARS-CoV-2感染对肾素-血管紧张素系统分子影响的模型
Modeling the molecular impact of SARS-CoV-2 infection on the renin-angiotensin system
摘要：
SARS-CoV-2冠状病毒感染是通过其刺突蛋白与血管紧张素转换酶2（ACE 2）结合介导的，ACE 2在肾素-血管紧张素系统（RAS）中起关键作用。研究SARS-CoV-2感染引起的RAS失调对于更好地理解COVID-19冠状病毒病的致病机制和危险因素以及设计有效的治疗策略至关重要。在这种情况下，我们开发了一个数学模型RAS的基础上的数据，蛋白质和肽的浓度，该模型进行了测试，从健康的血压正常和高血压的个人的临床数据。然后，我们使用我们的模型来分析SARS-CoV-2感染对RAS的影响，我们通过ACE 2下调作为病毒载量的函数来建模。我们还用它来预测RAS靶向药物（如RAS阻断剂、人重组ACE 2和血管紧张素1-7肽）对COVID-19患者的影响;该模型预测了一些药物的临床结局改善，而另一些药物的临床结局恶化。
英文摘要：
SARS-CoV-2 coronavirus infection is mediated by the binding of its spike protein to the angiotensin-converting enzyme 2 (ACE2), which plays a pivotal role in the renin-angiotensin system (RAS). The study of RAS dysregulation due to SARS-CoV-2 infection is fundamentally important for a better understanding of the pathogenic mechanisms and risk factors associated with COVID-19 coronavirus disease, and to design effective therapeutic strategies. In this context, we developed a mathematical model of RAS based on data regarding protein and peptide concentrations; the model was tested on clinical data from healthy normotensive and hypertensive individuals. We then used our model to analyze the impact of SARS-CoV-2 infection on RAS, which we modeled through a down-regulation of ACE2 as a function of viral load. We also used it to predict the effect of RAS-targeting drugs, such as RAS-blockers, human recombinant ACE2, and angiotensin 1-7 peptide, on COVID-19 patients; the model predicted an improvement of the clinical outcome for some drugs and a worsening for others.
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