囊性纤维化作为全身性疾病的数学模型。

IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
WIREs Mechanisms of Disease Pub Date : 2023-11-01 Epub Date: 2023-08-06 DOI:10.1002/wsbm.1625
Daniel V Olivença, Jacob D Davis, Carla M Kumbale, Conan Y Zhao, Samuel P Brown, Nael A McCarty, Eberhard O Voit
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引用次数: 0

摘要

囊性纤维化(CF)是一种众所周知的肺部疾病,尽管它实际上是一种系统性疾病,其症状通常首先表现为胃肠道功能障碍。CF最终不仅会损害胰腺和肠道,还会损害肺部、性腺、肝脏、肾脏、骨骼和心血管系统。它是由上皮离子通道蛋白CFTR基因的几个突变之一引起的。在过去的80年里,深入的研究和改进的抗菌治疗使CF患者的预期寿命从几周稳步增加到50岁以上 年。此外,近年来已有几种改善该疾病后遗症的药物问世,对该疾病根本原因的显著治疗最近使一些但并非所有pwCF的健康状况得到了显著改善。然而,许多根本问题仍未得到解答。使CF复杂化的事实是,例如在肺部,相关的氯化物分泌不足通常会扰乱上皮细胞的电化学平衡,并在气道中导致粘稠粘液和粘液斑块的积聚,这些粘液和粘液斑无法有效清除,并为一系列细菌和真菌群落提供了丰富的繁殖地。随后的感染往往是慢性的,对抗生素治疗的反应很差,结果有时与目标病原体的药物敏感性只有微弱的相关性。此外,与单一目标病原体快速解决的急性感染不同,慢性感染通常涉及多物种细菌群落,称为“感染微生物群”,它们发展自己的生态和进化动力学。目前还不可能设计出CF的整体数学模型,但为该疾病的许多不同驱动因素设计模型是可行的。在这些不断增长但又相互隔离的建模工作的基础上,我们在下文中讨论了多尺度建模框架(称为模板和锚点建模)的可行性,该框架允许逐步集成具有不同粒度的精细子模型。本文首先回顾了CF最重要的生物医学方面,随后描述了已经存在的或有可能加深我们对该疾病的多个方面及其相互关系的理解的数学建模方法。这里提出的方法背后的概念不仅与CF有关,而且可以转化为其他系统性疾病。本文分类在:先天性疾病>计算模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mathematical models of cystic fibrosis as a systemic disease.

Mathematical models of cystic fibrosis as a systemic disease.

Cystic fibrosis (CF) is widely known as a disease of the lung, even though it is in truth a systemic disease, whose symptoms typically manifest in gastrointestinal dysfunction first. CF ultimately impairs not only the pancreas and intestine but also the lungs, gonads, liver, kidneys, bones, and the cardiovascular system. It is caused by one of several mutations in the gene of the epithelial ion channel protein CFTR. Intense research and improved antimicrobial treatments during the past eight decades have steadily increased the predicted life expectancy of a person with CF (pwCF) from a few weeks to over 50 years. Moreover, several drugs ameliorating the sequelae of the disease have become available in recent years, and notable treatments of the root cause of the disease have recently generated substantial improvements in health for some but not all pwCF. Yet, numerous fundamental questions remain unanswered. Complicating CF, for instance in the lung, is the fact that the associated insufficient chloride secretion typically perturbs the electrochemical balance across epithelia and, in the airways, leads to the accumulation of thick, viscous mucus and mucus plaques that cannot be cleared effectively and provide a rich breeding ground for a spectrum of bacterial and fungal communities. The subsequent infections often become chronic and respond poorly to antibiotic treatments, with outcomes sometimes only weakly correlated with the drug susceptibility of the target pathogen. Furthermore, in contrast to rapidly resolved acute infections with a single target pathogen, chronic infections commonly involve multi-species bacterial communities, called "infection microbiomes," that develop their own ecological and evolutionary dynamics. It is presently impossible to devise mathematical models of CF in its entirety, but it is feasible to design models for many of the distinct drivers of the disease. Building upon these growing yet isolated modeling efforts, we discuss in the following the feasibility of a multi-scale modeling framework, known as template-and-anchor modeling, that allows the gradual integration of refined sub-models with different granularity. The article first reviews the most important biomedical aspects of CF and subsequently describes mathematical modeling approaches that already exist or have the potential to deepen our understanding of the multitude aspects of the disease and their interrelationships. The conceptual ideas behind the approaches proposed here do not only pertain to CF but are translatable to other systemic diseases. This article is categorized under: Congenital Diseases > Computational Models.

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WIREs Mechanisms of Disease
WIREs Mechanisms of Disease MEDICINE, RESEARCH & EXPERIMENTAL-
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