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Oxid Med Cell Longev. 2015;2015:732596. doi: 10.1155/2015/732596. Epub 2015 Oct 25.

Nrf2 Signaling and the Slowed Aging Phenotype: Evidence from Long-Lived Models.

Author information

1
Department of Health and Exercise Science, Colorado State University, 220 Moby B Complex, Fort Collins, CO 80523-1582, USA.

Abstract

Studying long-lived animals provides novel insight into shared characteristics of aging and represents a unique model to elucidate approaches to prevent chronic disease. Oxidant stress underlies many chronic diseases and resistance to stress is a potential mechanism governing slowed aging. The transcription factor nuclear factor (erythroid-derived 2)-like 2 is the "master regulator" of cellular antioxidant defenses. Nrf2 is upregulated by some longevity promoting interventions and may play a role in regulating species longevity. However, Nrf2 expression and activity in long-lived models have not been well described. Here, we review evidence for altered Nrf2 signaling in a variety of slowed aging models that accomplish lifespan extension via pharmacological, nutritional, evolutionary, genetic, and presumably epigenetic means.

PMID:
26583062
PMCID:
PMC4637130
DOI:
10.1155/2015/732596
[Indexed for MEDLINE]
Free PMC Article

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