Live longer on MARS: a yeast paradigm of mitochondrial adaptive ROS signaling in aging

Authors:

Gerald S. Shadel

doi: 10.15698/mic2014.05.143
Volume 1, pp. 140 to 144, published 23/04/2014.

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Affiliations:

Departments of Pathology and Genetics, Yale School of Medicine; New Haven, CT 06437-8023, USA.

Keywords: 

mitochondria, reactive oxygen species, epigenetic, hormesis, aging, ataxia-telangiectasia, signaling.

Corresponding Author(s):

Gerald S. Shadel, Departments of Pathology and Genetics, Yale School of Medicine; New Haven, CT 06437-8023, USA gerald.shadel@yale.edu

Conflict of interest statement:

The authors declare no conflict of interest.

Please cite this article as:

Gerald S. Shadel (2014). Live Longer on MARS: A Yeast Paradigm of Mitochondrial Adaptive ROS Signaling in Aging. Microbial Cell 1(5): 140-144.

© 2014 Shadel. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Adaptive responses to stress, including hormesis, have been implicated in longevity, but their mechanisms and outcomes are not fully understood. Here, I briefly summarize a longevity mechanism elucidated in the budding yeast chronological lifespan model by which Mitochondrial Adaptive ROS Signaling (MARS) promotes beneficial epigenetic and metabolic remodeling. The potential relevance of MARS to the human disease Ataxia-Telangiectasia and as a potential anti-aging target is discussed.