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Molecular inflammation hypothesis of aging based on the anti‐aging mechanism of calorie restriction
Author(s) -
Chung Hae Young,
Kim Hyon Jeen,
Kim Kyu Won,
Choi Jae Sue,
Yu Byung Pal
Publication year - 2002
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.10203
Subject(s) - inflammation , calorie restriction , oxidative stress , downregulation and upregulation , mechanism (biology) , senescence , oxidative phosphorylation , kinase , reactive oxygen species , biology , chemistry , microbiology and biotechnology , biochemistry , immunology , endocrinology , gene , philosophy , epistemology
Abstract Accumulating evidence strongly suggests that oxidative stress underlies aging processes. Research provides consistent evidence that calorie restriction (CR) reduces age‐related oxidative stress and has anti‐inflammatory properties. However, information is lacking on the molecular mechanism that would better define the interrelation of reactive oxygen species and nitrogen species and the pro‐inflammatory states of the aging process. In this review, the biochemical and molecular bases of the inflammatory process in the aging process are analyzed to delineate the molecular inflammation hypothesis of aging. The key players involved in the proposed hypothesis are the age‐related upregulation of NF‐κB, IL‐1β, IL‐6, TNFα, cyclooxygenase‐2, and inducible NO synthase, all of which are attenuated by CR. Furthermore, age‐related NFκB activation is associated with phosphorylation by IκB kinase/NIK and MAPKs, while CR blocked these activation processes. The modulation of these factors provides molecular insights of the anti‐inflammatory action of CR in relation to the aging process. Based on available finding and our recent supporting evidence, we prefer to use “molecular inflammation” to emphasize the importance of the molecular reaction mechanisms and their aberrance, predisposing to fully expressed chronic inflammatory phenomena. It was further proposed that CR's major force of the regulation of redox‐sensitive inflammation may well be its life‐prolonging action. Microsc. Res. Tech. 59:264–272, 2002. © 2002 Wiley‐Liss, Inc.