Abstract
Chronic inflammation, a pervasive feature of the aging process, is defined by a continuous, multifarious, low-grade inflammatory response. It is a sustained and systemic phenomenon that aggravates aging and can lead to age-related chronic diseases. In recent years, our understanding of age-related chronic inflammation has advanced through a large number of investigations on aging and calorie restriction (CR). A broader view of age-related inflammation is the concept of senoinflammation, which has an outlook beyond the traditional view, as proposed in our previous work. In this review, we discuss the effects of CR on multiple phases of proinflammatory networks and inflammatory signaling pathways to elucidate the basic mechanism underlying aging. Based on studies on senoinflammation and CR, we recognized that senescence-associated secretory phenotype (SASP), which mainly comprises cytokines and chemokines, was significantly increased during aging, whereas it was suppressed during CR. Further, we recognized that cellular metabolic pathways were also dysregulated in aging; however, CR mimetics reversed these effects. These results further support and enhance our understanding of the novel concept of senoinflammation, which is related to the metabolic changes that occur in the aging process. Furthermore, a thorough elucidation of the effect of CR on senoinflammation will reveal key insights and allow possible interventions in aging mechanisms, thus contributing to the development of new therapies focused on improving health and longevity.
Highlights
The aging process can be defined as progressive, physiological, functional deterioration throughout the lifetime of an individual by different convoluted interactions among genes and non-genetic environmental factors that eventually result in disruption of homeostasis and increased susceptibility to disease or death
The concept proposes a broader perspective on age-related inflammatory response and creates a complex network among many inflammatory mediators that can lead to systemic chronic inflammation
Oxidative stress leads to improper gene regulation and genomic DNA damage during aging
Summary
The aging process can be defined as progressive, physiological, functional deterioration throughout the lifetime of an individual by different convoluted interactions among genes and non-genetic environmental factors that eventually result in disruption of homeostasis and increased susceptibility to disease or death. The cell cycle of damaged cells, which cannot be recovered from cell death, is permanently arrested and the proliferative activity of these cells becomes extinct, which is defined as cellular senescence. This cellular response largely contributes to an organism’s aging. An increase in cellular dysregulation due to the release of proinflammatory molecules such as TNF, IL-1β, IL-6, MCP-1, MIP-1α, RANTES, and IL-18 [8,9] induces age-related chronic inflammation, leading to aging and its associated diseases. In order to understand age-related chronic inflammatory progress from a multilayered point of view, we previously proposed a novel concept of senoinflammation, which includes an expanded systemic view of chronic inflammation during the aging process. The beneficial effects of CR mimetics and other types of dietary restrictions on anti-aging are covered
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