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KMID : 0385220040140010012
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Korean Journal of Gerontology
2004 Volume.14 No. 1 p.12 ~ p.19
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Molecular Inflammation Hypothesis of Aging
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Chung Hae-Young
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Abstract
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A recent proposal of molecular inflammation hypothesis of the aging highlights this redox derangement as a plausible link between the normal aging process and age-related diseases. The hypothesis focused on the experimental observations revealing the dysregulated gene expression and transcription factors under the age-related oxidative stress. In review, the biochemical and molecular bases of the inflammatory process will be delineated as the possible molecular mechanism for the aging and the age-related diseases. The key players involved in the proposed mechanism are the age-related upregulation of NF-kB, IL-1b, IL-6, TNFa, cyclooxygenase-2, adhesion molecules and inducible NO synthase, all of which are attenuated by anti-aging calorie restriction (CR). Furthermore, data will be presented to describe molecular events leading to the age-related NF-kB activation with phosphorylation by IkB kinase/NIK and MAPKs, while CR blunted these activation process. Based on these and other recent evidence, we propose to use molecular inflammation to emphasize the increased molecular proinflammatory reactions with aging, thus predisposing the aged organism to fully expressed chronic inflammatory phenomena. This new proposal is in a full support of the current findings on the genomic, proteomic, and bioinformatic evidence about involvement of inflammation in the aging process.
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KEYWORD
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molecular inflammation, aging, calorie restriction
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