Molecular inflammation: underpinnings of aging and age-related diseases.
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.
Chung
Hae Young
HY
Department of Pharmacy, Longevity Science and Technology Institutes, Research Institute for Drug Development, Pusan National University, Geumjeong-gu, Busan 609-735, South Korea. hyjung@pusan.ac.kr
Cesari
Matteo
M
Anton
Stephen
S
Marzetti
Emanuele
E
Giovannini
Silvia
S
Seo
Arnold Young
AY
Carter
Christy
C
Yu
Byung Pal
BP
Leeuwenburgh
Christiaan
C
D000375:Aging / Q000502:physiology*; D000818:Animals; D004194:Disease / Q000209:etiology*; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000502:physiology; D008954:Models, Biological; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology
D018836:Inflammation Mediators