p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain
المؤلفون المشاركون
Carreras, María Cecilia
Pérez, Hernán
Finocchietto, Paola Vanesa
Alippe, Yael
Rebagliati, Inés
Elguero, María Eugenia
Villalba, Nerina
Poderoso, Juan José
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-03-12
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1212268
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر