Molecular Inflammation: Underpinnings of Aging and Age-related Diseases

By H. Chung, M. Cesari, S. Anton, E. Marzetti, S. Giovannini, Arnold Y. Seo, C. Carter, B. Yu, C. Leeuwenburgh. Ageing Research Reviews, 2008

1,180 citations recorded by the source corpus.

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) up-regulation of pro-inflammatory mediators (e.g., TNF-α, IL-1β, 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-κB 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.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1e81949202427b4eec19fbc029c61ac7b7eef3c0

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Citations in the corpus

JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age (2015, neutral): “system (53) or altered redox homeostasis (54).”
Role of ROS and Nutritional Antioxidants in Human Diseases (2018, background): “NF-κB is a key regulator for inflammatory factors such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6 (Chung et al., 2009).”
Inflammation and sarcopenia: A systematic review and meta-analysis. (2017, positive): “The oxidative stress-induced redox imbalance and the sustained upregulation of pro inflammatory mediators are believed to act as the patho-physiological basis underpinning inflammatory disorders including cardiovascular diseases, cancer, diabetes, dementia and also sarcopenia [1].”
Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases (2018, background): “The age-related redox imbalance is more likely triggered by the net effect of low antioxidative defense systems and incessantly produce of reactive species, including superoxide (O−2 ), hydroxyl radical (•OH), peroxynitrite (ONOO), hydrogen peroxide (H2O2), reactive lipid aldehydes, and reactive nit”
Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging (2009, background): “Chronic inf lammation is a major underlying condition of the aging process (32).”
Acute exercise and oxidative stress: a 30 year history (2009, background): “Moreover, because a more reducing environment is believed to promote healthenhancing effects [16], interventions designed to shift the redox balance in favor of greater reducing potential via increasing antioxidant defenses appears warranted.”
Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms (2011, background): “Scientists now recognize excessive and persistent inflammation as a contributor to the metabolic syndrome, CHD and stroke, autoimmune conditions, some cancers, and premature aging (Chung et al., 2009).”
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