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A mathematical model exhibiting the effect of DNA methylation on the stability boundary in cell-fate networks.展示 DNA 甲基化对细胞命运网络稳定性边界影响的数学模型。
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An upper limit on Gibbs energy dissipation governs cellular metabolism.吉布斯能耗散的上限控制着细胞代谢。
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A programmable fate decision landscape underlies single-cell aging in yeast.可编程的命运决策景观是酵母单细胞衰老的基础。
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Stochastic modeling reveals kinetic heterogeneity in post-replication DNA methylation.随机建模揭示复制后 DNA 甲基化中的动力学异质性。
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建模衰老及其对细胞功能和机体行为的影响。

Modeling aging and its impact on cellular function and organismal behavior.

机构信息

Department of Molecular Cellular and Developmental Biology, Yale University, 219 Prospect Street, New Haven, CT 06511, USA.

Department of Molecular Cellular and Developmental Biology, Yale University, 219 Prospect Street, New Haven, CT 06511, USA; Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT 06516, USA.

出版信息

Exp Gerontol. 2021 Nov;155:111577. doi: 10.1016/j.exger.2021.111577. Epub 2021 Sep 26.

DOI:10.1016/j.exger.2021.111577
PMID:34582969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8560568/
Abstract

Aging is a complex phenomenon of functional decay in a biological organism. Although the effects of aging are readily recognizable in a wide range of organisms, the cause(s) of aging are ill defined and poorly understood. Experimental methods on model organisms have driven significant insight into aging as a process, but have not provided a complete model of aging. Computational biology offers a unique opportunity to resolve this gap in our knowledge by generating extensive and testable models that can help us understand the fundamental nature of aging, identify the presence and characteristics of unaccounted aging factor(s), demonstrate the mechanics of particular factor(s) in driving aging, and understand the secondary effects of aging on biological function. In this review, we will address each of the above roles for computational biology in aging research. Concurrently, we will explore the different applications of computational biology to aging in single-celled versus multicellular organisms. Given the long history of computational biogerontological research on lower eukaryotes, we emphasize the key future goals of gradually integrating prior models into a holistic map of aging and translating successful models to higher-complexity organisms.

摘要

衰老是生物机体功能衰退的一种复杂现象。尽管衰老的影响在广泛的生物中很容易被识别,但衰老的原因仍未被明确界定和很好地理解。在模式生物上的实验方法推动了对衰老作为一个过程的深入了解,但并没有提供衰老的完整模型。计算生物学提供了一个独特的机会来解决我们知识中的这一差距,通过生成广泛和可测试的模型,帮助我们理解衰老的基本性质,识别未被考虑的衰老因素的存在和特征,展示特定因素在驱动衰老方面的机制,并了解衰老对生物功能的次要影响。在这篇综述中,我们将讨论计算生物学在衰老研究中的上述每一个作用。同时,我们将探讨计算生物学在单细胞和多细胞生物中对衰老的不同应用。鉴于计算生物老年学在低等真核生物上的悠久历史,我们强调了将先前的模型逐步整合到衰老的整体图谱中,并将成功的模型转化为更复杂的生物体的关键未来目标。