The roles of FoxOs in modulation of aging by calorie restriction

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• 作者：Dae Hyun Kim (1)
  Min Hi Park (1)
  Eun Kyeong Lee (1)
  Yeon Ja Choi (1)
  Ki Wung Chung (1)
  Kyoung Mi Moon (1)
  Min Jo Kim (1)
  Hye Jin An (1)
  June Whoun Park (1)
  Nam Deuk Kim (1)
  Byung Pal Yu (2)
  Hae Young Chung (1)
  
• 关键词：Aging ; Calorie restriction ; FoxO ; Age ; related diseases ; Oxidative stress
• 刊名：Biogerontology
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：16
• 期：1
• 页码：1-14
• 全文大小：398 KB
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• 作者单位：Dae Hyun Kim (1)
  Min Hi Park (1)
  Eun Kyeong Lee (1)
  Yeon Ja Choi (1)
  Ki Wung Chung (1)
  Kyoung Mi Moon (1)
  Min Jo Kim (1)
  Hye Jin An (1)
  June Whoun Park (1)
  Nam Deuk Kim (1)
  Byung Pal Yu (2)
  Hae Young Chung (1)
  
  1. Department of Pharmacy, Molecular Inflammation Research Center for Aging Intervention (MRCA), College of Pharmacy, Pusan National University, San 30, Jangjun-dong, Gumjung-gu, Busan, 609-735, Korea
  2. Department of Physiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Cell Biology
  Geriatrics and Gerontology
  Developmental Biology
  
• 出版者：Springer Netherlands
• ISSN：1573-6768

文摘

FoxO activity and modifications, such as its phosphorylation, acetylation, and methylation, may help drive the expression of genes involved in combating oxidative stress by causing the epigenetic modifications, and thus, preserve cellular function during aging and age-related diseases, such as diabetes, cancer, and Alzheimer disease. Insulin signaling has been postulated to influence the aging process by increasing resistance to oxidative stress, and slowing the accumulation of oxidative damage. Some antioxidative effects are mediated by a conserved family of forkhead box transcription factors (FoxOs), which in the absence of insulin signaling freely bind to promoters of antioxidant enzymes, superoxide dismutase, and catalase. On the other hand, calorie restriction (CR) extends the lifespans of several species via the insulin pathway, and extends longevity and healthspan in diverse species via a conserved mechanism. CR enhances adaptive stress responses at the cellular and organism levels and extends lifespan in a FoxO-independent manner. Thus, increased modification of FoxO is modulated via the hyperinsulinemia-induced PI3K/Akt pathway during aging, and CR reverses this process. Accordingly, FoxO plays an important role in maintenance of metabolic homeostasis and removal of oxidative stress in the aging process and in the effect of CR on lifespan.