| Literature DB >> 18692159 |
Hae Young Chung1, Matteo Cesari, Stephen Anton, Emanuele Marzetti, Silvia Giovannini, Arnold Young Seo, Christy Carter, Byung Pal Yu, Christiaan Leeuwenburgh.
Abstract
Recent scientific studies have advanced the notion of chronic inflammation as a major risk factor underlying aging and age-related diseases. In this review, low-grade, unresolved, molecular inflammation is described as an underlying mechanism of aging and age-related diseases, which may serve as a bridge between normal aging and age-related pathological processes. Accumulated data strongly suggest that continuous (chronic) upregulation of pro-inflammatory mediators (e.g., TNF-alpha, IL-1beta, IL-6, COX-2, iNOS) are induced during the aging process due to an age-related redox imbalance that activates many pro-inflammatory signaling pathways, including the NF-kappaB signaling pathway. These pro-inflammatory molecular events are discussed in relation to their role as basic mechanisms underlying aging and age-related diseases. Further, the anti-inflammatory actions of aging-retarding caloric restriction and exercise are reviewed. Thus, the purpose of this review is to describe the molecular roles of age-related physiological functional declines and the accompanying chronic diseases associated with aging. This new view on the role of molecular inflammation as a mechanism of aging and age-related pathogenesis can provide insights into potential interventions that may affect the aging process and reduce age-related diseases, thereby promoting healthy longevity.Entities:
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Year: 2008 PMID: 18692159 PMCID: PMC3782993 DOI: 10.1016/j.arr.2008.07.002
Source DB: PubMed Journal: Ageing Res Rev ISSN: 1568-1637 Impact factor: 10.895