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整合计算和生物学血流动力学方法,改进动脉粥样硬化血管建模。

Integrating Computational and Biological Hemodynamic Approaches to Improve Modeling of Atherosclerotic Arteries.

机构信息

Graduate School of Biomedical Engineering, University of New South Wales, Sydney, 2052, Australia.

Department of Functional Materials in Medicine and Dentistry, Institute of Functional Materials and Biofabrication (IFB), KeyLab Polymers for Medicine of the Bavarian Polymer Institute (BPI), University of Würzburg, Pleicherwall 2, 97070, Würzburg, Germany.

出版信息

Adv Sci (Weinh). 2024 Jul;11(26):e2307627. doi: 10.1002/advs.202307627. Epub 2024 May 5.

DOI:10.1002/advs.202307627
PMID:38704690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11234431/
Abstract

Atherosclerosis is the primary cause of cardiovascular disease, resulting in mortality, elevated healthcare costs, diminished productivity, and reduced quality of life for individuals and their communities. This is exacerbated by the limited understanding of its underlying causes and limitations in current therapeutic interventions, highlighting the need for sophisticated models of atherosclerosis. This review critically evaluates the computational and biological models of atherosclerosis, focusing on the study of hemodynamics in atherosclerotic coronary arteries. Computational models account for the geometrical complexities and hemodynamics of the blood vessels and stenoses, but they fail to capture the complex biological processes involved in atherosclerosis. Different in vitro and in vivo biological models can capture aspects of the biological complexity of healthy and stenosed vessels, but rarely mimic the human anatomy and physiological hemodynamics, and require significantly more time, cost, and resources. Therefore, emerging strategies are examined that integrate computational and biological models, and the potential of advances in imaging, biofabrication, and machine learning is explored in developing more effective models of atherosclerosis.

摘要

动脉粥样硬化是心血管疾病的主要原因,导致个人及其社区的死亡率上升、医疗保健成本增加、生产力下降和生活质量降低。由于对其根本原因的理解有限,以及当前治疗干预措施的局限性,情况更加恶化,这突出了对复杂动脉粥样硬化模型的需求。本综述批判性地评估了动脉粥样硬化的计算和生物学模型,重点研究了粥样硬化冠状动脉中的血液动力学。计算模型考虑了血管和狭窄的几何复杂性和血液动力学,但它们无法捕捉动脉粥样硬化涉及的复杂生物学过程。不同的体外和体内生物学模型可以捕捉健康和狭窄血管的生物学复杂性的某些方面,但很少模拟人体解剖结构和生理血液动力学,并且需要更多的时间、成本和资源。因此,研究了整合计算和生物学模型的新兴策略,并探讨了成像、生物制造和机器学习方面的进展在开发更有效的动脉粥样硬化模型方面的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/e582d484c942/ADVS-11-2307627-g015.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/d57af2f11d0f/ADVS-11-2307627-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/510e3faade26/ADVS-11-2307627-g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/44acca7e64b0/ADVS-11-2307627-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/d73e0ea9d02a/ADVS-11-2307627-g021.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4e/11234431/e582d484c942/ADVS-11-2307627-g015.jpg

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ScRNA-seq and spatial transcriptomics: exploring the occurrence and treatment of coronary-related diseases starting from development.
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