2015
DOI: 10.1007/s10522-015-9585-9
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Mitochondrial responsibility in ageing process: innocent, suspect or guilty

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Cited by 62 publications
(40 citation statements)
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References 223 publications
(237 reference statements)
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“…Therefore, we assume that XS cells, which are unable to store trehalose, might be defective in the adaptation to stress conditions, which explains their poor vitality. Trehalose is formed while cells are undergoing the shift from fermentative to respiratory metabolism (Futcher 2006), and it was shown that the trehalose pathway regulates mitochondrial respiratory chain content (Noubhani et al 2009, López-Lluch et al 2015). Since XS cells have very low respiration capacity, it points to defects in trehalose metabolism.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, we assume that XS cells, which are unable to store trehalose, might be defective in the adaptation to stress conditions, which explains their poor vitality. Trehalose is formed while cells are undergoing the shift from fermentative to respiratory metabolism (Futcher 2006), and it was shown that the trehalose pathway regulates mitochondrial respiratory chain content (Noubhani et al 2009, López-Lluch et al 2015). Since XS cells have very low respiration capacity, it points to defects in trehalose metabolism.…”
Section: Discussionmentioning
confidence: 99%
“…Some identified exogenous triggers include smoking (Behnia et al, 2016), air pollution (Fougere et al, 2015), persistent infections (Derhovanessian et al, 2011; Oppermann et al, 2012) and overweight or obesity (Giugliano et al, 2006). Several endogenous factors also play a relevant role, including: overproduction of reactive oxygen species (ROS) (Zhang et al, 2016) and advanced glycation end-products (AGEs) (Yamagishi and Matsui, 2016), mitochondrial dysfunction (Lopez-Lluch et al, 2015), renin-angiotensin system (RAS) deregulation (Duprez, 2006), hormonal changes (Epel and Lithgow, 2014; Gubbels Bupp, 2015), visceral adiposity (Palmer and Kirkland, 2016), changes in the gut microbiota (Biagi et al, 2010) and accumulation of cell debris due to a defective autophagy (Franceschi et al, 2016). …”
Section: Introductionmentioning
confidence: 99%
“…Oxidative stress and mitochondrial dysfunction are well known to increase during aging [1214] including brain aging [15, 16] and are considered a major cause for cellular senescence [1719]. During aging, neurons are exposed to high oxidative stress and accumulate dysfunctional mitochondria, damage to DNA, proteins and lipids and changes in energy homeostasis [16, 20].…”
Section: Introductionmentioning
confidence: 99%