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A regulated response to mitochondrial dysfunction modulates longevity and rates of living

dc.contributor.advisorCarneiro, Jorge
dc.contributor.authorCristina, David Zeferino d’Azevedo
dc.date.accessioned2010-08-23T14:00:19Z
dc.date.available2010-08-23T14:00:19Z
dc.date.issued2008-12
dc.description.abstractAging is a long-standing biological question of tremendous social and cultural importance. Despite this, only in the last 15 years has biology started to make significant progress in understanding the underlying mechanisms that regulate aging. This progress stemmed mainly from the use of model organisms, which allowed the discovery of several genes directly modulating longevity. Interestingly, several of these longevity genes are necessary for normal mitochondrial function, and disruption of their activity delays the aging process. This is somewhat paradoxical, considering the importance of cellular respiration for energy production and viability of eukaryotic organisms. One possible rationalization for this is that by decreasing cellular respiration, reactive oxygen species (ROS) generation is also reduced, and in that way, cellular decay and aging are delayed.(...)en_US
dc.identifier.urihttp://hdl.handle.net/10362/4079
dc.language.isoengen_US
dc.publisherUniversidade Nova de Lisboa. Instituto de Tecnologia Química e Biológicaen_US
dc.titleA regulated response to mitochondrial dysfunction modulates longevity and rates of livingen_US
dc.typedoctoral thesis
dspace.entity.typePublication
my.embargo.termsnullen_US
rcaap.rightsopenAccessen_US
rcaap.typedoctoralThesisen_US

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