2014
DOI: 10.1016/j.cell.2014.10.039
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Abstract: Mammalian aging can be delayed with genetic, dietary and pharmacologic approaches. Given that the elderly population is dramatically increasing and that aging is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, it is critical to expand Geroscience research directed at extending human healthspan.

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Cited by 1,704 publications
(1,295 citation statements)
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References 15 publications
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“…In fact, the reduced rates of mitophagy observed in KIFC3 depleted cells can explain the abnormal morphology of the mitochondria compartment previously described upon KIFC3 knockdown (Dietrich, Seiler, Essmann & Dodt, 2013). Thus, loss of KIFC3 leads to reduced autophagic activity and perturbed mitochondria morphology/content, two well‐described features of old cells (Kennedy et al., 2014; Lopez‐Otin et al., 2013) .…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In fact, the reduced rates of mitophagy observed in KIFC3 depleted cells can explain the abnormal morphology of the mitochondria compartment previously described upon KIFC3 knockdown (Dietrich, Seiler, Essmann & Dodt, 2013). Thus, loss of KIFC3 leads to reduced autophagic activity and perturbed mitochondria morphology/content, two well‐described features of old cells (Kennedy et al., 2014; Lopez‐Otin et al., 2013) .…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, genetic inhibition of this degradative process recapitulates features associated with aging and age‐related diseases (Hara et al., 1997; Komatsu et al., 2006, 2007; Menzies et al., 2017). Loss of protein/organelle quality control is a universal hallmark of aging, and malfunctioning of autophagy with age contributes to this gradual accumulation of damaged proteins and dysfunctional organelles (Kaushik & Cuervo, 2015; Kennedy et al., 2014; Lopez‐Otin, Blasco, Partridge, Serrano & Kroemer, 2013). However, the cellular and molecular mechanisms underlying this progressive decline in autophagy during aging remain unknown.…”
Section: Introductionmentioning
confidence: 99%
“…Aging is one of the greatest risk factors for many diseases, and it ultimately restricts the lifespan of organisms by increasing the probability of death (Dillin, Gottschling & Nystrom, 2014; Guarente, Ruvkun & Amasino, 1998; Kennedy et al., 2014; Kenyon, 2005; Niccoli & Partridge, 2012). Since the discovery and characterization of the first long‐lived mutants in Caenorhabditis elegans and Saccharomyces cerevisiae more than two decades ago (Kaeberlein, McVey & Guarente, 1999; Kenyon, Chang, Gensch, Rudner & Tabtiang, 1993; Morris, Tissenbaum & Ruvkun, 1996; Ogg et al., 1997; Wang et al., 1993), the concept that aging is a malleable biological process has been well embraced (Finch & Ruvkun, 2001; Gems & Partridge, 2013; Kennedy, 2008; Kenyon, 2005, 2010).…”
Section: Research Organisms For Agingmentioning
confidence: 99%
“…This view is now changed. As the intrinsic biological mechanism of aging is slowly revealed, there is hope that interventions that slow aging and prevent or delay the onset of chronic disease and functional impairments can be discovered (Kennedy et al., 2014; Lopez‐Otin, Blasco, Partridge, Serrano, & Kroemer, 2013). …”
Section: Introductionmentioning
confidence: 99%