Bifurcation and stability analysis of atherosclerosis disease model characterizing the anti-oxidative activity of HDL during short- and long-time evolution

Asish Adak, Debasmita Mukherjee, Praveen Kumar Gupta
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Abstract

Abstract In this article, a partial differential equation (PDE) model for atherosclerosis disease is presented that analyzes the anti-oxidative activity of high-density lipoprotein (HDL) during the reverse cholesterol transport (RCT) process. The model thoroughly investigates the complex interplay between oxidized low-density lipoprotein (ox-LDL) and high-density lipoprotein in the context of atherosclerosis, emphasizing their combined impact on plaque formation, disease progression, and regression. In addition to this, we considered that monocytes are also attracted by the presence of ox-LDL within the intima. Detailed discussions on stability analyses of the reaction dynamical system at non-inflammatory and chronic equilibrium are provided, followed by a bifurcation analysis for the proposed system. Furthermore, stability analysis for the PDE model in the presence of diffusion is conducted. Our study reveals that the oxidation rate of LDL by monocytes (δ) and the influx rate of HDL (ϕ) due to drugs/diet are primarily responsible for the existence of bi-stability of equilibrium points. In the numerical results, we observe that non-inflammatory or chronic equilibrium points exist for either a short or a long time, and these findings are validated with existing results. The biological elucidation shows the novelty in terms of enhancing our ability to assess intervention efficacy to generate therapeutic strategies resulting in the reduction of the atherosclerotic burden and associated cardiovascular risks.
动脉粥样硬化疾病模型的分岔和稳定性分析,表征高密度脂蛋白在短期和长期演变过程中的抗氧化活性
摘要 本文提出了一个动脉粥样硬化疾病的偏微分方程(PDE)模型,分析了高密度脂蛋白(HDL)在胆固醇反向运输(RCT)过程中的抗氧化活性。该模型深入研究了动脉粥样硬化背景下氧化低密度脂蛋白(ox-LDL)和高密度脂蛋白之间复杂的相互作用,强调了它们对斑块形成、疾病进展和消退的共同影响。除此之外,我们还考虑到单核细胞也会被内膜中存在的 ox-LDL 所吸引。我们详细讨论了反应动力学系统在非炎症平衡和慢性平衡时的稳定性分析,随后对提出的系统进行了分岔分析。此外,还对存在扩散的 PDE 模型进行了稳定性分析。我们的研究发现,单核细胞对低密度脂蛋白的氧化率(δ)和药物/饮食导致的高密度脂蛋白流入率(j)是平衡点双稳态存在的主要原因。在数值结果中,我们观察到非炎症或慢性平衡点存在的时间或长或短,这些发现与现有结果相吻合。生物学上的阐明显示了其新颖性,有助于提高我们评估干预效果的能力,从而制定治疗策略,减少动脉粥样硬化的负担和相关的心血管风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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