Journal
EXPERIMENTAL GERONTOLOGY
Volume 35, Issue 5, Pages 521-532Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0531-5565(00)00118-2
Keywords
atherosclerosis; peroxisome proliferator; nuclear factor kappa B
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Funding
- NIAID NIH HHS [R37 AI 20866, R37 AI020866, R01 AI020866] Funding Source: Medline
- NIA NIH HHS [R01 AG019519, R37 AG 10486] Funding Source: Medline
- NIDDK NIH HHS [DK 14744] Funding Source: Medline
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A progressive rise of oxidative stress due to the altered redox homeostasis appears to be one of the hallmarks of the aging process. Reactive oxygen species (ROS) also serve as signaling agents for inflammation, a systemic defensive reaction against microbial pathogens and other foreign bodies. Changes in the pattern of gene expression through ROS-sensitive transcription factors give rise to both aging and inflammation phenotypes, Chronic oxidative stress and inflammatory reaction also lead to many age-associated diseases such as atherosclerosis and arthritis. Transcription factors that are directly influenced by ROS and proinflammatory cytokines include nuclear factor kappa B (NF-kappa B), activator protein 1 (AP-1), specificity protein 1 (Sp1), peroxisome proliferator-activated receptors (PPARs) and other members of the nuclear receptor superfamily. Here we describe the basic components of the intracellular redox control machinery and their dysregulation with age leading to altered transcription factor function and age-associated pathophysiology. (C) 2000 Elsevier Science Inc. All rights reserved.
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