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Open AccessJournal ArticleDOI

NAD(+) Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus.

TLDR
This review summarizes how NAD(+) metabolism links energy status with adaptive cellular and organismal responses and how this knowledge can be therapeutically exploited.
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This article is published in Cell Metabolism.The article was published on 2015-07-07 and is currently open access. It has received 1061 citations till now. The article focuses on the topics: Mitochondrial unfolded protein response & NAD+ kinase.

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Citations
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Journal ArticleDOI

The Mitochondrial Basis of Aging

TL;DR: It is suggested that mitochondria influence or regulate a number of key aspects of aging and suggest that strategies directed at improving mitochondrial quality and function might have far-reaching beneficial effects.
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NAD+ in aging, metabolism, and neurodegeneration

TL;DR: Factors that regulate NAD+ and how supplementation with NAD+ precursors may represent a new therapeutic opportunity for aging and its associated disorders, particularly neurodegenerative diseases are reviewed.
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NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

TL;DR: It is demonstrated the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence and it is demonstrated that NR delays senescences of neural SCs and melanocyteSCs and increases mouse life span.
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Kynurenines: Tryptophan’s metabolites in exercise, inflammation, and mental health

TL;DR: The modulation of tryptophan-kynurenine metabolism using lifestyle and pharmacological interventions could help prevent and treat several diseases with underlying inflammatory mechanisms, including metabolic, oncologic, and mental health disorders.
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NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR

TL;DR: A comprehensive concept that connects NAD+ metabolism to the control of aging and longevity in mammals has been proposed, and the stage is now set to test whether these exciting preclinical results can be translated to improve human health.
References
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Journal ArticleDOI

Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

TL;DR: BRCA1 or BRCA2 dysfunction unexpectedly and profoundly sensitizes cells to the inhibition of PARP enzymatic activity, resulting in chromosomal instability, cell cycle arrest and subsequent apoptosis, illustrating how different pathways cooperate to repair damage.
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Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

TL;DR: It is proposed that, in the absence of PARP1, spontaneous single-strand breaks collapse replication forks and trigger homologous recombination for repair and exploited in order to kill BRCA2-deficient tumours by PARP inhibition alone.
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Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase

TL;DR: The analysis of two SIR2 mutations supports the idea that this deacetylase activity accounts for silencing, recombination suppression and extension of life span in vivo, and provides a molecular framework of NAD-dependent histone de acetylation that connects metabolism, genomic silencing and ageing in yeast and, perhaps, in higher eukaryotes.
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