The genetics of ageing

By C. Kenyon. Nature, 2010

2,753 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Physiology

View Paper: https://www.semanticscholar.org/paper/e98104b2ce1c520b33c3668aaeb2e34794261b9e

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Citations in the corpus

Mitonuclear protein imbalance as a conserved longevity mechanism (2013, background): “We focused on the mitochondrial pathway, because (1) it robustly effects longevity(22); (2) MRPs function in the translation of mtDNAencoded oxidative phosphorylation subunits(6,7); and (3) in the BXDs, Mrps5 networked with several oxidative phosphorylation components (Fig.”
Low Protein Intake is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population (2014, neutral): “The effect of the insulin/IGF-1 pathway on longevity was ﬁrst described in C. elegans by showing that mutations in the insulin/IGF-1 receptor or in the downstream age-1 gene caused a several-fold increase in lifespan (Johnson, 1990; Kenyon et al., 1993, Kenyon, 2010).”
Promoting Health and Longevity through Diet: from Model Organisms to Humans (2015, neutral): “, 2014), and growth hormone in themouse (Johnson et al., 2013; Kenyon, 2010).”
In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming (2016, neutral): “The last decade of scientiﬁc research has dramatically improved our understanding of the aging process (Johnson et al., 2013; Kenyon, 2010; Riera et al., 2016).”
Sirt1 extends life span and delays aging in mice through the regulation of Nk2 homeobox 1 in the DMH and LH. (2013, background): “These regulators and signaling pathways, including insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) (Kenyon, 2010), mammalian target of rapamycin (mTOR) signaling (Zoncu et al., 2011), and NAD-dependent sirtuins (Haigis and Sinclair, 2010), provide excellent probes to dissect complex hie”
mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “Conversely, suppression of growth programmes through chemical and genetic manipulations, or by reducing food intake, results in the activation of salvage programmes that preserve the functionality of cells and tissues for extended periods of time (reviewed in Ref”
Ageing as a risk factor for disease. (2012, background): “Moderately reduced mitochondrial activity can increase lifespan in yeast, worms, flies and mice [10], although the exact mechanisms at work await discovery.”
The sirtuin SIRT6 regulates lifespan in male mice (2012, background): “Gene expression analysis revealed significant differences between male Sirt6 -transgenic mice and male wild-type mice: transgenic males displayed lower serum levels of insulin-like growth factor 1 (IGF1), higher levels of IGF-binding protein 1 and altered phosphorylation levels of major components ”
The hallmarks of aging. (2013, background): “…or downstream intracellular effectors such as AKT,mTOR, and FOXO have been linked to longevity, both in humansand inmodel organisms, further illustrating themajor impact of trophic and bioenergetic pathways on longevity (Barzilai et al., 2012; Fontana et al., 2010; Kenyon, 2010) (Figure 4A).”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “Diverse approaches including different dietary regimens or using compounds that mimic dietary restriction have been employed to investigate the effect of dietary restriction on lifespan extension in C. elegans (Kenyon, 2010b).”