A growing number of evidences indicate a strict causality between the reduction of autophagic functionality and aging. In this context the preservation of a proper autophagic response is of paramount importance to preserve the cellular processes in aging cell. Nutrients availability, especially for amino acids, is the most physiological key regulator of macroautophagy. In mammalian cells the knowledge of the mechanism and the underlying regulation of macroautophagy has been greatly improved in recent years and we focus on the role of nutrients, in particular on their involvement in preventing cellular aging through the modulation of autophagy. This review covers the main features of macroautophagy regulation by nutrients, in particular amino acids as well as glucose and vitamins, and its mechanisms, focusing primarily on the mammalian hepatocyte, which has been extensively utilized to dissect signaling pathways underlying the regulation of macroautophagy.

Nutrient control of macroautophagy in mammalian cells.

MIOTTO, GIOVANNI
2006

Abstract

A growing number of evidences indicate a strict causality between the reduction of autophagic functionality and aging. In this context the preservation of a proper autophagic response is of paramount importance to preserve the cellular processes in aging cell. Nutrients availability, especially for amino acids, is the most physiological key regulator of macroautophagy. In mammalian cells the knowledge of the mechanism and the underlying regulation of macroautophagy has been greatly improved in recent years and we focus on the role of nutrients, in particular on their involvement in preventing cellular aging through the modulation of autophagy. This review covers the main features of macroautophagy regulation by nutrients, in particular amino acids as well as glucose and vitamins, and its mechanisms, focusing primarily on the mammalian hepatocyte, which has been extensively utilized to dissect signaling pathways underlying the regulation of macroautophagy.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2439285
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 73
  • ???jsp.display-item.citation.isi??? 0
  • OpenAlex ND
social impact