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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 732596, 15 pages
Review Article

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

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

Received 8 April 2015; Revised 28 May 2015; Accepted 4 June 2015

Academic Editor: Claudio Cabello-Verrugio

Copyright © 2015 Danielle R. Bruns et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.