A mathematical model for atherosclerotic plaque formation and arterial wall remodelling

动脉壁 内皮 纤维帽 内科学 血管造影 易损斑块 心脏病学 医学
作者
Md. Hamidul Islam,Peter R. Johnston
出处
期刊:Australian & New Zealand industrial and applied mathematics journal [Australian Mathematical Publishing Association, Inc.]
卷期号:57: 320-320 被引量:12
标识
DOI:10.21914/anziamj.v57i0.10386
摘要

Atherosclerosis is a condition whereby fatty material is deposited in the walls of arteries (plaque) resulting in a thickening of the wall. Here we develop a mathematical model describing the biochemical processes of the formation of atherosclerotic plaque, which involves the interaction between pro-inflammatory mediators, modified low density lipoprotein, monocytes, macrophages, foam cells and high density lipoprotein. In addition, based on the outcomes of the biochemical model, we develop a plaque growth model that takes into account both the inward and outward expansion of the arterial walls. We examine the stability and bifurcations of this model in order to explore the clinical and medical implications of plaque growth. References M. J. van Gils and D. Vukadinovic, A. C. van Dijk, D. W. J. Dippel, W. J. Niessen and A. van der Lugt. Carotid atherosclerotic plaque progression and change in plaque composition over time: A 5-year follow-up study using serial CT angiography. Am. J. Neuroradiol., 37(7):1267–1273, 2012. doi:10.3174/ajnr.A2970 M. Naghavi, P. Libby, E. Falk, et al. From vulnerable plaque to vulnerable patient; A call for new definitions and risk assessment strategies: Part I. Circulation, 108(14):1664–1672, 2003. doi:10.1161/01.CIR.0000087480.94275.97 T. F. Lucher and M. Barton. Biology of the Endothelium. Clin Cardiol., 20(Supp. 2):3–10, 1997. https://www.researchgate.net/profile/Matthias_Barton/publication/13807118_Biology_of_the_endothelium/links/0046352c54fe700895000000.pdf E. Mannarino and M. Pirro. Endothelial injury and repair: A novel theory for atherosclerosis. Angiology, 59:69S-72S, 2008. doi:10.1177/0003319708320761 C. Davis, J. Fischer, K. Ley and I. J. Sarembock. The role of inflammation in vascular injury and repair. J. Thromb. Haemost., 1(8):1699-1709, 2003. doi:10.1046/j.1538-7836.2003.00292.x G. K. Hansson and P. Libby. The immune response in atherosclerosis: a double-edged sword. Nat. Rev. Immunol., 6(7):508–519, 2006. doi:10.1038/nri1882 R. Ross. Atherosclerosis–-an inflammatory disease, New Engl. J. Med., 340(2):115-126, 1999. doi:10.1056/NEJM199901143400207 B. F. Asztalos. High-density lipoprotein metabolism and progression of atherosclerosis: new insights from the HDL atherosclerosis treatment study. Curr. Opin. Cardiol., 19(4):385–391, 2004. http://journals.lww.com/co-cardiology/Abstract/2004/07000/High_density_lipoprotein_metabolism_and.16.aspx N. El Khatib, S. Genieys and V. Volpert. Atherosclerosis initiation modeled as an inflammatory process. Math. Model. Nat. Phenom., 2(2):126–141, 2007. doi:10.1051/mmnp:2008022 P.-W. Fok. Mathematical model of intimal thickening in atherosclerosis: Vessel stenosis as a free boundary problem. J. Theor. Biol., 314:23–33, 2012. doi:10.1016/j.jtbi.2012.07.029 M. A. K. Bulelzai and J. L. A. Dubbeldam. Long time evolution of atherosclerotic plaques, J. Theor. Biol., 297:1–10, 2012. doi:10.1016/j.jtbi.2011.11.023 A. D. Chalmers, A. Cohen, C. A. Bursill and M. R. Myerscough. Bifurcation and dynamics in a mathematical model of early atherosclerosis. J. Math. Biol., 71:1451–1480, 2015. doi:10.1007/s00285-015-0864-5 A. Friedman and W. Hao. A mathematical model of atherosclerosis with reverse cholesterol transport and associated risk factors. B. Math. Biol., 77(5):758–781, 2015. doi:10.1007/s11538-014-0010-3 G. M. Chisolm, S. L. Hazen, P. L. Fox and M. K. Cathcart. The oxidation of lipoproteins by monocytes-macrophages: Biochemical and biological mechanisms. J. Biol. Chem., 274(37):25959–25962, 1999. doi:10.1074/jbc.274.37.2595 A. Daugherty, N. R. Webb, D. L. Rateri and V. L. King. Thematic review series: The immune system and atherogenesis. Cytokine regulation of macrophage functions in atherogenesis, J. Lipid Res., 46(9):1812-1822, 2005. doi:10.1194/jlr.R500009-JLR200 L. J. H. van Tits, R. Stienstra, P. L. van Lent, M. G. Netea, L. A. B. Joosten and A. F. H. Stalenhoef. Oxidized LDL enhances pro-inflammatory responses of alternatively activated M2 macrophages: A crucial role for Kruppel-like factor 2. Atherosclerosis, 214(8):345–349, 2011. doi:10.1016/j.atherosclerosis.2010.11.018 Z. Mallat, S. Besnard, M. Duriez, et al. Protective role of interleukin-10 in atherosclerosis. Circ. Res., 85(8):e17-e24, 1999. doi:10.1161/01.RES.85.8.e17 P. J. Barter, S. Nicholls, K.-A. Rye, G. M. Anantharamaiah, M. Navab and A. M. Fogelman. Antiinflammatory properties of HDL, Circ. Res., 95(8):764–772, 2004. doi:10.1161/01.RES.0000146094.59640.13 M. Sanson, E. Distel and E. A. Fisher. HDL induces the expression of the M2 macrophage markers arginase 1 and Fizz-1 in a STAT6-dependent process. PLoS One, 8(8):e74676, 2013. doi:10.1371/journal.pone.0074676 L. Tilling, J. Hunt, A. Donald, B. Clapp and P. Chowienczyk. Arterial injury and endothelial repair: Rapid recovery of function after mechanical injury in healthy volunteers. Card. Res. Prac., 2014:367537, 2014. doi:10.1155/2014/367537 F. Alexandrea, V. H. S. Zagoa, N. B. Panzoldo, et al. Reference values for high-density lipoprotein particle size and volume by dynamic light scattering in a Brazilian population sample and their relationships with metabolic parameters. Clin. Chim. Acta, 442:63–72, 2015. doi:10.1016/j.cca.2015.01.006 T. Khamdaeng, J. Luo, J. Vappou, P. Terdtoon, E. E. Konofagou. Arterial stiffness identification of the human carotid artery using the stress-strain relationship in vivo. Ultrasonics, 52(3):402–411, 2012. doi:10.1016/j.ultras.2011.09.006 T. G. Kuznetsova, M. N. Starodubtseva, N. I. Yegorenkov, S. A. Chizhik, R. I. Zhdanov. Atomic force microscopy probing of cell elasticity, Micron., 38(8):824–833, 2007, doi:10.1016/j.micron.2007.06.011 J. Bell, C. Breward, T. Chou, P.-W. Fok, J. M. Haugh, Q. Li, L. Rossi, A. Walter, X. Yang, A. Zemlyanova and N. Zhang. Mathematical models for vulnerable plaques. Technical Report, 2009. http://www.maths-in-industry.org/miis/272/ A. Dhooge, W. Govaerts and Y. A. Kuznetsov. MATCONT: a MATLAB package for numerical bifurcation analysis of ODEs. ACM T. Math. Softw. (TOMS), 29(2):141–164, 2003. doi:10.1145/779359.779362. R. Ross. The pathogenesis of atherosclerosis: A perspective for the 1990s. Nature, 362:801–809, 1993. doi:10.1038/362801a0.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
biomds发布了新的文献求助10
1秒前
JasonYang举报Pf1314求助涉嫌违规
1秒前
1秒前
1秒前
1秒前
所所应助高高亦竹采纳,获得10
2秒前
2秒前
3秒前
Wangyn完成签到,获得积分10
3秒前
林曦发布了新的文献求助10
3秒前
4秒前
奶黄包发布了新的文献求助10
4秒前
JasonYang应助呐小王搞科研采纳,获得10
5秒前
Z_jx完成签到,获得积分10
5秒前
5秒前
显隐发布了新的文献求助10
6秒前
显隐发布了新的文献求助10
6秒前
显隐发布了新的文献求助10
6秒前
7秒前
司空晋鹏发布了新的文献求助10
7秒前
王兴龙发布了新的文献求助10
7秒前
Andrew完成签到,获得积分10
8秒前
茶茶发布了新的文献求助10
8秒前
顺心的筮发布了新的文献求助10
10秒前
10秒前
11秒前
宁123完成签到,获得积分10
12秒前
biomds完成签到,获得积分10
13秒前
13秒前
蛐蛐发布了新的文献求助10
14秒前
烟花应助马俊杰采纳,获得10
14秒前
小华发布了新的文献求助10
15秒前
16秒前
16秒前
科研通AI6应助刁刁采纳,获得10
16秒前
17秒前
研六六完成签到,获得积分10
17秒前
18秒前
18秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Teaching Language in Context (Third Edition) 1000
Identifying dimensions of interest to support learning in disengaged students: the MINE project 1000
Introduction to Early Childhood Education 1000
List of 1,091 Public Pension Profiles by Region 921
Aerospace Standards Index - 2025 800
流动的新传统主义与新生代农民工的劳动力再生产模式变迁 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 物理化学 基因 遗传学 催化作用 冶金 量子力学 光电子学
热门帖子
关注 科研通微信公众号,转发送积分 5436097
求助须知:如何正确求助?哪些是违规求助? 4548199
关于积分的说明 14212530
捐赠科研通 4468375
什么是DOI,文献DOI怎么找? 2448993
邀请新用户注册赠送积分活动 1439942
关于科研通互助平台的介绍 1416594