کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1902209 1534307 2016 15 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Nrf2 signaling and redox homeostasis in the aging heart: A potential target to prevent cardiovascular diseases?
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Nrf2 signaling and redox homeostasis in the aging heart: A potential target to prevent cardiovascular diseases?
چکیده انگلیسی


• Aged population in the world will increase dramatically in the next years.
• Cardiovascular diseases will remain the leading cause of death in the elderly.
• Oxidative stress contributes to cardiovascular disease in aging.
• Nrf2 activity enhancement may reduce the burden of cardiovascular diseases in elderly.

Aging process is often accompanied with a high incidence of cardiovascular diseases (CVD) due to the synergistic effects of age-related changes in heart morphology/function and prolonged exposure to injurious effects of CVD risk factors. Oxidative stress, considered a hallmark of aging, is also an important feature in pathologies that predispose to CVD development, like hypertension, diabetes and obesity. Approaches directed to prevent the occurrence of CVD during aging have been explored both in experimental models and in controlled clinical trials, in order to improve health span, reduce hospitalizations and increase life quality during elderly. In this review we discuss oxidative stress role as a main risk factor that relates CVD with aging. As well as interventions that aim to reduce oxidative stress by supplementing with exogenous antioxidants. In particular, strategies of improving the endogenous antioxidant defenses through activating the nuclear factor related-2 factor (Nrf2) pathway; one of the best studied molecules in cellular redox homeostasis and a master regulator of the antioxidant and phase II detoxification response.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Ageing Research Reviews - Volume 26, March 2016, Pages 81–95
نویسندگان
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