title: Molecular inflammation as an underlying mechanism of the aging process and age-related diseases.
abstract: Aging is a biological process characterized by time-dependent functional declines that are influenced by changes in redox status and by oxidative stress-induced inflammatory reactions. An organism's pro-inflammatory status may underlie the aging process and age-related diseases. In this review, we explore the molecular basis of low-grade, unresolved, subclinical inflammation as a major risk factor for exacerbating the aging process and age-related diseases. We focus on the redox-sensitive transcription factors, NF-κB and FOXO, which play essential roles in the expression of pro-inflammatory mediators and anti-oxidant enzymes, respectively. Major players in molecular inflammation are discussed with respect to the age-related up-regulation of pro-inflammatory cytokines and adhesion molecules, cyclo-oxygenase-2, lipoxygenase, and inducible nitric oxide synthase. The molecular inflammation hypothesis proposed by our laboratory is briefly described to give further molecular insights into the intricate interplay among redox balance, pro-inflammatory gene activation, and chronic age-related inflammatory diseases. The final section discusses calorie restriction as an aging-retarding intervention that also exhibits extraordinarily effective anti-inflammatory activity by modulating GSH redox, NF-κB, SIRT1, PPARs, and FOXOs.
authors: Molecular Inflammation Research Center for Aging Intervention, Pusan National University, Busan 609-735, Korea. hyjung@pusan.ac.kr
authors: H Y
authors: HY
authors: Chung
authors: E K
authors: EK
authors: Lee
authors: Y J
authors: YJ
authors: Choi
authors: J M
authors: JM
authors: Kim
authors: D H
authors: DH
authors: Kim
authors: Y
authors: Y
authors: Zou
authors: C H
authors: CH
authors: Kim
authors: J
authors: J
authors: Lee
authors: H S
authors: HS
authors: Kim
authors: N D
authors: ND
authors: Kim
authors: J H
authors: JH
authors: Jung
authors: B P
authors: BP
authors: Yu
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism; D031204:Caloric Restriction; D015815:Cell Adhesion Molecules / Q000378:metabolism; D055113:Chronic Periodontitis / Q000378:metabolism; D051858:Forkhead Transcription Factors / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D008084:Lipoxygenase / Q000378:metabolism; D024821:Metabolic Syndrome / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010024:Osteoporosis / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D015815:Cell Adhesion Molecules; D051858:Forkhead Transcription Factors; D018836:Inflammation Mediators; D016328:NF-kappa B; D008084:Lipoxygenase; D052247:Nitric Oxide Synthase Type II; D011451:Prostaglandin-Endoperoxide Synthases