When less is more: hormesis against stress and disease
Authors:Andreas Zimmermann1, Maria A. Bauer1, Guido Kroemer2-5, Frank Madeo1 and Didac Carmona-Gutierrez1
1 Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria.
2 Equipe 11 Labellisée Ligue Contre le Cancer, INSERM U1138, Centre de Recherche des Cordeliers, 15 Rue de l’École de Médecine, 75006 Paris, France.
3 Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Pavillon de Recherche 1, 94805 Villejuif, France.
4 Université Paris Descartes, Sorbonne Paris Cité, 12 Rue de l’École de Médecine, 75006 Paris, France.
5 Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, 20 Rue Leblanc, 75015 Paris, France.
Keywords:
hormesis, stress resistance, aging, neurodegeneration, therapeutic preconditioning.
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Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Andreas Zimmermann, Maria A. Bauer, Guido Kroemer, Frank Madeo and Didac Carmona-Gutierrez (2014). When less is more: hormesis against stress and disease. Microbial Cell 1(5): 150-153.
© 2014 Zimmermann et al. 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:
All living organisms need to adapt to ever changing adverse conditions in order to survive. The phenomenon termed hormesis describes an evolutionarily conserved process by which a cell or an entire organism can be preconditioned, meaning that previous exposure to low doses of an insult protects against a higher, normally harmful or lethal dose of the same stressor. Growing evidence suggests that hormesis is directly linked to an organism’s (or cell’s) capability to cope with pathological conditions such as aging and age-related diseases. Here, we condense the conceptual and potentially therapeutic importance of hormesis by providing a short overview of current evidence in favor of the cytoprotective impact of hormesis, as well as of its underlying molecular mechanisms.
doi: 10.15698/mic2014.05.148
Volume 1, pp. 150 to 153, published 05/05/2014.