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Review
, 8 (1), 18-30

Molecular Inflammation: Underpinnings of Aging and Age-Related Diseases

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Review

Molecular Inflammation: Underpinnings of Aging and Age-Related Diseases

Hae Young Chung et al. Ageing Res Rev.

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.

Figures

Fig. 1
Fig. 1
Major molecular pro-inflammatory pathways involved in aging and age-related diseases. ROS, reactive oxygen species; MAPK, mitogen-activated protein kinases, NIK, NFκ-B-induced kinase; IKK, IκB kinase; AMs, adhesion molecules; iNOS, inducible NO synthase; COX-2, cyclooxygenase.
Fig. 2
Fig. 2
The role of inflammation in pathophysiological process and the possible action of CR and exercise. CR, calorie restriction.

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