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.

Molecular inflammation : underpinnings of aging and age-related diseases / H.Y. Chung, M. Cesari, S. Anton, E. Marzetti, S. Giovannini, A.Y. Seo, C. Carter, B.P. Yu, C. Leeuwenburgh. - In: AGEING RESEARCH REVIEWS. - ISSN 1568-1637. - 8:1(2009), pp. 18-30.

Molecular inflammation : underpinnings of aging and age-related diseases

M. Cesari;
2009

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.
Age-related diseases; Aging; Atherosclerosis; Calorie restriction; Cancer; Cytokines; Dementia; Exercise; Inflammatory diseases; Molecular inflammation; Obesity; Osteoporosis; Oxidative stress; Sarcopenia; Aging; Animals; Disease; Humans; Inflammation; Inflammation Mediators; MAP Kinase Signaling System; Models, Biological; Oxidation-Reduction; Oxidative Stress; Biotechnology; Biochemistry; Aging; Molecular Biology; Neurology
Settore MED/09 - Medicina Interna
2009
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/550993
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