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Hormesis, cellular stress response and vitagenes as critical determinants in aging and longevity

Calabrese, Vittorio, Cornelius, Carolin, Cuzzocrea, Salvatore, Iavicoli, Ivo, Rizzarelli, Enrico, Calabrese, Edward J.·2011·Molecular Aspects of Medicine
DOI 10.1016/j.mam.2011.10.007
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Abstract

Understanding mechanisms of aging and determinants of life span will help to reduce age-related morbidity and facilitate healthy aging. Average lifespan has increased over the last centuries, as a consequence of medical and environmental factors, but maximal life span remains unchanged. Extension of maximal life span is currently possible in animal models with measures such as genetic manipulations and caloric restriction (CR). CR appears to prolong life by reducing reactive oxygen species (ROS)-mediated oxidative damage. But ROS formation, which is positively implicated in cellular stress response mechanisms, is a highly regulated process controlled by a complex network of intracellular signaling pathways. By sensing the intracellular nutrient and energy status, the functional state of mitochondria, and the concentration of ROS produced in mitochondria, the longevity network regulates life span across species by co-ordinating information flow along its convergent, divergent and multiply branched signaling pathways, including vitagenes which are genes involved in preserving cellular homeostasis during stressful conditions. Vitagenes encode for heat shock proteins (Hsp) Hsp32, Hsp70, the thioredoxin and the sirtuin protein systems. Dietary antioxidants, such as carnosine, carnitines or polyphenols, have recently been demonstrated to be neuroprotective through the activation of hormetic pathways, including vitagenes. The hormetic dose-response, challenges long-standing beliefs…

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  • Mild toxic treatments trigger beneficial compensatory responses that surpass the repair of the triggering damage and improve cellular fitness compared to pre-damage conditions.

    “mild toxic treatments trigger beneficial compensatory responses that surpass the repair of the triggering damage, and actually produce an improvement in cellular fitness when compared to the starting pre-damage conditions”

    From The Hallmarks of Aging (2013) · cites this paper as Calabrese et al., 2011

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Metadata

Authors
Calabrese, V., Cornelius, C., Cuzzocrea, S., Iavicoli, I., Rizzarelli, E., & Calabrese, E. J.
Venue
Molecular Aspects of Medicine
Publisher
Elsevier BV
Published
2011-08
Volume
32
Issue
4-6
Pages
279-304
ISSN
0098-2997
DOI
10.1016/j.mam.2011.10.007
Cited by
197
References
9
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • MIUR
  • FIRB RBRN07BMCT
  • I.N.B.B.
  • ‘‘Fondi Ateneo’’ 2008 and 2009

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