Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival.
By Hongying Yang, Tianle Yang, Joseph A. Baur, Evelyn J. Perez, T. Matsui, J. Carmona, Dudley Lamming, N. Souza-Pinto, V. Bohr, A. Rosenzweig and 3 more. Cell, 2007
949 citations recorded by the source corpus.
Subfields: Epidemiology, Geriatrics and Gerontology, Physiology
View Paper: https://www.semanticscholar.org/paper/a4cc9e2ccd0453f7078c7ada7750201cbeb55b7f
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Citations in the corpus
- CD38 dictates age-related NAD decline and mitochondrial dysfunction through a SIRT3-dependent mechanism (2016, neutral): “It has been shown that the cellular NAD pool is determined by a balance between the activity of NAD-synthesizing and NAD-consuming enzymes (Aksoy et al., 2006; Bai et al., 2011; Barbosa et al., 2007; Nahimana et al., 2009; Yang et al., 2007; Yoshino et al., 2011).”
- Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “Under stress and nutrient restriction conditions, NAM phosphoribosyltransferase (NAMPT) is induced and protects cells against death induced by genotoxic stress in a SIRT3- and SIRT4-dependent manner (Yang et al., 2007).”
- The NAD+ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet induced obesity (2012, positive): “Given the existence of different cellular NAD+ pools and the relevance of mitochondrial NAD+ content for mitochondrial and cellular function (Yang et al., 2007a), we also analyzed whether NR treatment would affect mitochondrial NAD+ levels.”
- Sirtuin Regulation of Mitochondria - Energy Production, Apoptosis, and Signaling (2010, background): “For example, in the cellular response to DNA damage when mitochondrial NAD+ levels fall below critical levels, SIRT3 and SIRT4 display anti-apoptotic activity, protecting cells from death [64].”
- Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. (2009, background): “The levels of Nampt have been shown to be upregulated during mild stress of cardiomyocytes, thus supporting the possibility of involvement of the NAD salvage pathway in the regulation of SIRT1 levels during mild stress situations (34).”