Calorie restriction, SIRT1 and metabolism: understanding longevity

By Laura Bordone, L. Guarente. Nature reviews. Molecular cell biology, 2005

1,021 citations recorded by the source corpus.

Subfields: Aging, Geriatrics and Gerontology, Physiology

View Paper: https://www.semanticscholar.org/paper/aeed1c1e973dce9dc37ef204e7e2e72786b6b1bf

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Citations in the corpus

SIRT1 controls endothelial angiogenic functions during vascular growth. (2007, background): “Although SIRTs have been shown to play a critical role in the regulation of several essential physiological processes (Bordone and Guarente 2005), little information is available on a putative role of SIRTs in endothelial and vascular homeostasis.”
The NAD+-Dependent Deacetylase SIRT1 Modulates CLOCK-Mediated Chromatin Remodeling and Circadian Control (2008, neutral): “These proteins are structurally distinct from the other HDACs and have the property of dynamically sensing cellular energy metabolism (Bordone and Guarente, 2005).”
SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis (2007, background): “including caloric restriction, which has been shown to prevent numerous diseases of aging in mammals such as Alzheimer’s disease (AD) (Lamming et al, 2004; Bordone and Guarente, 2005; Lombard et al, 2005).”
Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012, background): “Improved glucose tolerance and insulin sensitivity are hallmarks of CR in mammals, and a common feature of many models of increased longevity (12-16), although mice lacking insulin receptor substrate (IRS) proteins 1 or 2 provide a notable counterexample (17, 18).”
Lifespan and reproduction in Drosophila: New insights from nutritional geometry (2008, background): “It is widely held that the life-extending effects of dietary restriction (DR) are due to caloric restriction (CR) (1, 8, 9), but recently this view has been challenged by experiments suggesting that specific nutrients (proteins and certain amino acids) rather than energy are responsible (10–12).”
SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “…resveratrol, SRT1720, or overexpression of SIRT1 has been shown to activate PGC-1α and prevent diseases commonly associated with mitochondrial dysfunction and aging (Banks et al., 2008; Baur et al., 2006; Bordone and Guarente, 2005; Herranz et al., 2010; Lagouge et al., 2006; Pearson et al., 2008).”
Sirt1 Regulates Insulin Secretion by Repressing UCP2 in Pancreatic β Cells (2005, neutral): “In one example, mitochondria from UCP3 KO mice generated higher levels of superoxide [53,54], suggesting that some degree of uncoupling can be beneficial by controlling reactive oxygen species production [55].”
Human Ageing Genomic Resources: new and updated databases (2017, background): “Examples of these include WRN, the mutation of which results in Werner syndrome, possibly the most dramatic progeroid syndrome (5), LMNA, the mutation of which leads to Hutchinson-Gilford’s progeroid syndrome (6), and SIRT1, linked to several processes involved in ageing (7) (Figure 1).”
Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α (2007, background): “Nutrient or caloric restriction results in major tissuespecific metabolic changes that ultimately cause an increase of longevity in many different organisms (Bordone and Guarente, 2005; Sinclair, 2005).”
Early aging and age-related pathologies in mice deficient in BMAL1, the core componentof the circadian clock. (2006, background): “…sensitivity in Bmal1−/− animals (Rudic et al. 2004) suggests a possible connection between the circadian system and the insulin/insulin growth factor (IGF) pathways, which are known to be involved in the control of lifespan in different organisms (Bordone and Guarente 2005; Katic and Kahn 2005).”