The life span-prolonging effect of Sirtuin-1 is mediated by autophagy

Morselli, Eugenia; Maiuri, Maria Chiara; Markaki, Maria; Megalou, Evgenia; Pasparaki, Angela; Palikaras, Konstantinos; Criollo, Alfredo; Galluzzi, Lorenzo; Malik, Shoaib Ahmad; Vitale, Ilio; Michaud, Mickaël; Madeo, Frank; Tavernarakis, Nektarios; Kroemer, Guido

doi:10.4161/auto.6.1.10817

Cited by 134 publications

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“…Furthermore, certain beneficial effects of calorie restriction may be driven by this metabolic modulator. In fact, calorie restriction is associated with an increase in mitochondrial turnover (41). Our results support the previous notion by other reports that, under conditions of calorie restriction, the maintenance of a high [NAD ϩ ]/[NADH] ratio elevates the rate of mitochondrial turnover through the activation of SIRT1.…”

Section: Discussionsupporting

confidence: 92%

“…More importantly, the treatment of the activators, similar to the One important message of our study is that the activation of SIRT1 causes a decrease in the cellular content of mitochondria through the induction of autophagy and mitochondrial fragmentation. Previous studies showed that SIRT1 overexpression or its activation by resveratrol (although the effect of resveratrol may also be mediated by AMP-activated protein kinase activation (31)) induces autophagy (21,41). SIRT1 has also been shown to play an essential role in the induction of autophagy in fasting cardiac myocytes (42).…”

Section: Discussionmentioning

confidence: 99%

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Nicotinamide-induced Mitophagy

Jang

Kang

Hwang

2012

Journal of Biological Chemistry

221

103

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Nicotinamide-induced Mitophagy

Jang

Kang

Hwang

2012

Journal of Biological Chemistry

221

103

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“…Transgenic expression of sir-2.1 induces autophagy in C. elegans. Interestingly, deletion or depletion of Atg6/bec-1 not only suppresses the induction of autophagy by sir-2.1 but also abrogates longevity in these worms (Morselli et al, 2010a). In addition, activation of SIR-2.1 by transgenic overexpression of pnc-1, a gene encoding the pyrazinamidase/nicotinamidase PNC-1 that catabolizes nicotinamide, a sirtuin inhibitor, also extends lifespan in C. elegans.…”

Section: Sirtuinsmentioning

confidence: 99%

Autophagy and ageing: Insights from invertebrate model organisms

Lionaki

Markaki

Tavernarakis

2013

Ageing Research Reviews

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a b s t r a c tAgeing in diverse species ranging from yeast to humans is associated with the gradual, lifelong accumulation of molecular and cellular damage. Autophagy, a conserved lysosomal, self-destructive process involved in protein and organelle degradation, plays an essential role in both cellular and whole-animal homeostasis. Accumulating evidence now indicates that autophagic degradation declines with age and this gradual reduction of autophagy might have a causative role in the functional deterioration of biological systems during ageing. Indeed, loss of autophagy gene function significantly influences longevity. Moreover, genetic or pharmacological manipulations that extend lifespan in model organisms often activate autophagy. Interestingly, conserved signalling pathways and environmental factors that regulate ageing, such as the insulin/IGF-1 signalling pathway and oxidative stress response pathways converge on autophagy. In this article, we survey recent findings in invertebrates that contribute to advance our understanding of the molecular links between autophagy and the regulation of ageing. In addition, we consider related mechanisms in other organisms and discuss their similarities and idiosyncratic features in a comparative manner.

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“…Both caloric restriction and resveratrol require sirtuin-1, a deacetylase, to promote lifespan extension [167,168]. Interestingly, sirtuin-1, apart from targeting histones, also targets key Atg proteins, such as Atg5, Atg7 and Atg8, and its overexpression induces autophagy [169,170]. Similarly, spermidine triggers epigenetic deacetylation through inhibition of acetyltransferases and, in addition, prevents oxidative stress and necrosis [171].…”

Section: Autophagy and Ageingmentioning

confidence: 99%

Autophagy: for better or for worse

et al. 2011

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Autophagy is a lysosomal degradation pathway that degrades damaged or superfluous cell components into basic biomolecules, which are then recycled back into the cytosol. In this respect, autophagy drives a flow of biomolecules in a continuous degradation-regeneration cycle. Autophagy is generally considered a pro-survival mechanism protecting cells under stress or poor nutrient conditions. Current research clearly shows that autophagy fulfills numerous functions in vital biological processes. It is implicated in development, differentiation, innate and adaptive immunity, ageing and cell death. In addition, accumulating evidence demonstrates interesting links between autophagy and several human diseases and tumor development. Therefore, autophagy seems to be an important player in the life and death of cells and organisms. Despite the mounting knowledge about autophagy, the mechanisms through which the autophagic machinery regulates these diverse processes are not entirely understood. In this review, we give a comprehensive overview of the autophagic signaling pathway, its role in general cellular processes and its connection to cell death. In addition, we present a brief overview of the possible contribution of defective autophagic signaling to disease.

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The life span-prolonging effect of Sirtuin-1 is mediated by autophagy

Cited by 134 publications

References 0 publications

Nicotinamide-induced Mitophagy

Nicotinamide-induced Mitophagy

Autophagy and ageing: Insights from invertebrate model organisms

Autophagy: for better or for worse

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