Alterations in the target of the rapamycin (TOR) nutrient-sensing pathway are thought to contribute to physiological aging. In normal conditions the activity of the pathway is promoted by mitogens, growth factors, and nutrients (in particular amino acids) thus regulating diverse fundamental functions such as cell growth, proliferation, development, memory, angiogenesis, autophagy, and immune responses. Through life hyperactivation of the mTOR complexes is associated with more rapid aging, whereas hypoactivation leads to reduced translation and increased longevity in several animal species.

mTOR, nutrition and ageing

D'ANTONA, GIUSEPPE
2016-01-01

Abstract

Alterations in the target of the rapamycin (TOR) nutrient-sensing pathway are thought to contribute to physiological aging. In normal conditions the activity of the pathway is promoted by mitogens, growth factors, and nutrients (in particular amino acids) thus regulating diverse fundamental functions such as cell growth, proliferation, development, memory, angiogenesis, autophagy, and immune responses. Through life hyperactivation of the mTOR complexes is associated with more rapid aging, whereas hypoactivation leads to reduced translation and increased longevity in several animal species.
2016
Molecular basis of nutrition and ageing
Marco Malavolta and Eugenio Mocchegiani, editors
Physiology considers resources that study the regulation of biological functions at the level of the whole organism. This includes research from biochemical, cell biological and whole system studies of human and animal physiology. Comparative physiology, biological rhythms, and physiological measurement are also included. Resources emphasizing cellular regulation, or the physiology of specific organs are excluded and are covered in the Cell & Developmental Biology and Medical Research: Organs & Systems categories.
Comitato scientifico
Inglese
141
153
13
9780128018163
Elsevier
2 Contributo in Volume::2.1 Contributo in volume (Capitolo o Saggio)
1
268
none
D'Antona, Giuseppe
info:eu-repo/semantics/bookPart
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/1126861
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