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dc.contributor.authorMc Auley, Mark T.*
dc.contributor.authorMooney, Kathleen M.*
dc.contributor.authorAngell, Peter J.*
dc.contributor.authorWilkinson, Stephen J.*
dc.date.accessioned2015-05-01T15:30:26Z
dc.date.available2015-05-01T15:30:26Z
dc.date.issued2015-04-27
dc.identifier.citationMc Auley, M. T., Mooney, K. M., Angell, P. J., Wilkinson, S. J. (2015). Mathematical modelling of metabolic regulation in aging. Metabolites, 2015, 5, pp. 232-251en
dc.identifier.issn2218-1989en
dc.identifier.doi10.3390/metabo5020232
dc.identifier.urihttp://hdl.handle.net/10034/551062
dc.description.abstractThe 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.
dc.language.isoenen
dc.publisherMDPIen
dc.relation.urlhttp://www.mdpi.com/journal/metabolitesen
dc.relation.urlhttp://www.mdpi.com/2218-1989/5/2/232en
dc.subjectsystems biologyen
dc.subjectagingen
dc.subjectcomputational modellingen
dc.subjectmammalian target of rapamycinen
dc.subjectsimulationen
dc.subjectsirtuinsen
dc.subjectSIRT1en
dc.subjectregulatory networken
dc.titleMathematical modelling of metabolic regulation in agingen
dc.typeArticleen
dc.contributor.departmentUniversity of Chester ; Liverpool Hope University ; Edge Hill University ; University of Chesteren
dc.identifier.journalMetabolites
refterms.dateFOA2018-08-13T12:44:57Z
html.description.abstractThe 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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