Mathematical Modelling of Metabolic Regulation in Aging

Mark T. Mc Auley; Kathleen M. Mooney; Peter J. Angell; Stephen J. Wilkinson

doi:10.3390/metabo5020232

Mathematical Modelling of Metabolic Regulation in Aging

Mark T. Mc Auley, Kathleen M. Mooney, Peter J. Angell, Stephen J. Wilkinson

Allied Health, Social Work & Wellbeing

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Abstract

The underlying cellular mechanisms that characterize aging are complex and multifaceted. However, it is emerging that aging could be regulated by two distinct metabolic hubs. These hubs are the pathway defined by the mammalian target of rapamycin (mTOR) and that defined by the NAD+-dependent deacetylase enzyme, SIRT1. Recent experimental evidence suggests that there is crosstalk between these two important pathways; however, the mechanisms underpinning their interaction(s) remains poorly understood. In this review, we propose using computational modelling in tandem with experimentation to delineate the mechanism(s). We briefly discuss the main modelling frameworks that could be used to disentangle this relationship and present a reduced reaction pathway that could be modelled. We conclude by outlining the limitations of computational modelling and by discussing opportunities for future progress in this area

Original language	English
Pages (from-to)	232-251
Journal	Metabolites
Volume	5
Issue number	2
Early online date	27 Apr 2015
DOIs	https://doi.org/10.3390/metabo5020232
Publication status	E-pub ahead of print - 27 Apr 2015

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title = "Mathematical Modelling of Metabolic Regulation in Aging",

abstract = "The underlying cellular mechanisms that characterize aging are complex and multifaceted. However, it is emerging that aging could be regulated by two distinct metabolic hubs. These hubs are the pathway defined by the mammalian target of rapamycin (mTOR) and that defined by the NAD+-dependent deacetylase enzyme, SIRT1. Recent experimental evidence suggests that there is crosstalk between these two important pathways; however, the mechanisms underpinning their interaction(s) remains poorly understood. In this review, we propose using computational modelling in tandem with experimentation to delineate the mechanism(s). We briefly discuss the main modelling frameworks that could be used to disentangle this relationship and present a reduced reaction pathway that could be modelled. We conclude by outlining the limitations of computational modelling and by discussing opportunities for future progress in this area",

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year = "2015",

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T1 - Mathematical Modelling of Metabolic Regulation in Aging

AU - Mc Auley, Mark T.

AU - Mooney, Kathleen M.

AU - Angell, Peter J.

AU - Wilkinson, Stephen J.

PY - 2015/4/27

Y1 - 2015/4/27

N2 - The underlying cellular mechanisms that characterize aging are complex and multifaceted. However, it is emerging that aging could be regulated by two distinct metabolic hubs. These hubs are the pathway defined by the mammalian target of rapamycin (mTOR) and that defined by the NAD+-dependent deacetylase enzyme, SIRT1. Recent experimental evidence suggests that there is crosstalk between these two important pathways; however, the mechanisms underpinning their interaction(s) remains poorly understood. In this review, we propose using computational modelling in tandem with experimentation to delineate the mechanism(s). We briefly discuss the main modelling frameworks that could be used to disentangle this relationship and present a reduced reaction pathway that could be modelled. We conclude by outlining the limitations of computational modelling and by discussing opportunities for future progress in this area

AB - The underlying cellular mechanisms that characterize aging are complex and multifaceted. However, it is emerging that aging could be regulated by two distinct metabolic hubs. These hubs are the pathway defined by the mammalian target of rapamycin (mTOR) and that defined by the NAD+-dependent deacetylase enzyme, SIRT1. Recent experimental evidence suggests that there is crosstalk between these two important pathways; however, the mechanisms underpinning their interaction(s) remains poorly understood. In this review, we propose using computational modelling in tandem with experimentation to delineate the mechanism(s). We briefly discuss the main modelling frameworks that could be used to disentangle this relationship and present a reduced reaction pathway that could be modelled. We conclude by outlining the limitations of computational modelling and by discussing opportunities for future progress in this area

U2 - 10.3390/metabo5020232

DO - 10.3390/metabo5020232

M3 - Article (journal)

VL - 5

SP - 232

EP - 251

JO - Metabolites

JF - Metabolites

IS - 2

ER -

Mathematical Modelling of Metabolic Regulation in Aging

Abstract

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