![](/images/graphics-bg.png)
p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain
Joint Authors
Carreras, María Cecilia
Pérez, Hernán
Finocchietto, Paola Vanesa
Alippe, Yael
Rebagliati, Inés
Elguero, María Eugenia
Villalba, Nerina
Poderoso, Juan José
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-03-12
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Programmed and damage aging theories have traditionally been conceived as stand-alone schools of thought.
However, the p66Shc adaptor protein has demonstrated that aging-regulating genes and reactive oxygen species (ROS) are closely interconnected, since its absence modifies metabolic homeostasis by providing oxidative stress resistance and promoting longevity.
p66Shc(−/−) mice are a unique opportunity to further comprehend the bidirectional relationship between redox homeostasis and the imbalance of mitochondrial biogenesis and dynamics during aging.
This study shows that brain mitochondria of p66Shc(−/−) aged mice exhibit a reduced alteration of redox balance with a decrease in both ROS generation and its detoxification activity.
We also demonstrate a strong link between reactive nitrogen species (RNS) and mitochondrial function, morphology, and biogenesis, where low levels of ONOO− formation present in aged p66Shc(−/−) mouse brain prevent protein nitration, delaying the loss of biological functions characteristic of the aging process.
Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(−/−) brain mitochondria.
Low levels of protein nitration and acetylation could cause the metabolic homeostasis maintenance observed during aging in this group, thus increasing its lifespan.
American Psychological Association (APA)
Pérez, Hernán& Finocchietto, Paola Vanesa& Alippe, Yael& Rebagliati, Inés& Elguero, María Eugenia& Villalba, Nerina…[et al.]. 2018. p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-13.
https://search.emarefa.net/detail/BIM-1212268
Modern Language Association (MLA)
Pérez, Hernán…[et al.]. p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-13.
https://search.emarefa.net/detail/BIM-1212268
American Medical Association (AMA)
Pérez, Hernán& Finocchietto, Paola Vanesa& Alippe, Yael& Rebagliati, Inés& Elguero, María Eugenia& Villalba, Nerina…[et al.]. p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-13.
https://search.emarefa.net/detail/BIM-1212268
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1212268