Bifurcation and stability analysis of atherosclerosis disease model characterizing the anti-oxidative activity of HDL during short- and long-time evolution
{"title":"Bifurcation and stability analysis of atherosclerosis disease model characterizing the anti-oxidative activity of HDL during short- and long-time evolution","authors":"Asish Adak, Debasmita Mukherjee, Praveen Kumar Gupta","doi":"10.1515/zna-2023-0331","DOIUrl":null,"url":null,"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.","PeriodicalId":23871,"journal":{"name":"Zeitschrift für Naturforschung A","volume":"52 12","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zeitschrift für Naturforschung A","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/zna-2023-0331","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.