Journal
REDOX BIOLOGY
Volume 5, Issue -, Pages 71-79Publisher
ELSEVIER
DOI: 10.1016/j.redox.2015.03.004
Keywords
Redox systems biology; Oxidative stress; Redox signaling
Categories
Funding
- NIH [AG038746, ES023485, HL113451, ES009047, ES019776]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P20HL113451] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES009047, T32ES012870, R01ES023485, P30ES019776] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG038746] Funding Source: NIH RePORTER
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Metazoan genomes encode exposure memory systems to enhance survival and reproductive potential by providing mechanisms for an individual to adjust during lifespan to environmental resources and challenges. These systems are inherently redox networks, arising during evolution of complex systems with O-2 as a major determinant of bioenergetics, metabolic and structural organization, defense, and reproduction. The network structure decreases flexibility from conception onward due to differentiation and cumulative responses to environment (exposome). The redox theory of aging is that aging is a decline in plasticity of genome-exposome interaction that occurs as a consequence of execution of differentiation and exposure memory systems. This includes compromised mitochondrial and bioenergetic flexibility, impaired food utilization and metabolic homeostasis, decreased barrier and defense capabilities and loss of reproductive fidelity and fecundity. This theory accounts for hallmarks of aging, including failure to maintain oxidative or xenobiotic defenses, mitochondrial integrity, proteostasis, barrier structures, DNA repair, telomeres, immune function, metabolic regulation and regenerative capacity. (C) 2015 Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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