Angiotensin II Type 1 Receptor Autoantibodies (AT1-AA) as a functional receptor activator can persistently activate Angiotensin II Type 1 Receptor (AT1R) by causing AT1R non-desensitization which is one of the important pathogenesis of preeclampsia (PE). However, the molecular mechanisms of AT1-AA results AT1R non-desensitization remain unknown. In order to explore the background molecular mechanisms of AT1R non-desensitization induced by AT1-AA, we construct dynamical models which are composed of control model (based on the body of healthy pregnant women) and experimental group models (based on the body of pregnant women with PE) in this paper. We also consider the effect of membrane fluidity on the reaction when building the dynamical models. In the experiment group models, we establish two models that caused AT1R non-desensitization: endocytosis disorder model and conformational change model. We write C++ and MATLAB programs to do the data fitting. By comparing the data fitting results and analyzing the images of models and corresponding Bayesian information criterion (BIC) values, we conclude that conformational changes may be the key molecular mechanism of AT1R non-desensitization.

中文翻译：

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鉴定AT1R不脱敏的主要分子机制

血管紧张素 II 1 型受体自身抗体 (AT1-AA) 作为功能性受体激活剂可以持续激活血管紧张素 II 1 型受体 (AT1R) 通过引起 AT1R非脱敏是先兆子痫(PE)的重要发病机制之一。然而，AT1-AA 的分子机制导致 AT1R 非脱敏仍然未知。为了探索AT的背景分子机制1本文构建了由AT1-AA诱导的R非脱敏模型，由对照模型（基于健康孕妇身体）和实验组模型（基于PE孕妇身体）组成。在建立动力学模型时，我们还考虑了膜流动性对反应的影响。在实验组模型中，我们建立了两个导致 AT1R非脱敏：内吞障碍模型和构象变化模型。我们编写 C++ 和 MATLAB 程序来进行数据拟合。通过比较数据拟合结果，分析模型图像和相应的贝叶斯信息准则（BIC）值，我们得出结论，构象变化可能是AT的关键分子机制。1R 非脱敏。