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

Abstract EN

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.