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Review
. 2016:2016:3565127.
doi: 10.1155/2016/3565127. Epub 2016 May 10.

ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases

Pierpaola Davalli  1 , Tijana Mitic  2 , Andrea Caporali  3 , Angela Lauriola  1 , Domenico D'Arca  4
Affiliations
Review

ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases

Pierpaola Davalli et al. Oxid Med Cell Longev. 2016.

Abstract

The aging process worsens the human body functions at multiple levels, thus causing its gradual decrease to resist stress, damage, and disease. Besides changes in gene expression and metabolic control, the aging rate has been associated with the production of high levels of Reactive Oxygen Species (ROS) and/or Reactive Nitrosative Species (RNS). Specific increases of ROS level have been demonstrated as potentially critical for induction and maintenance of cell senescence process. Causal connection between ROS, aging, age-related pathologies, and cell senescence is studied intensely. Senescent cells have been proposed as a target for interventions to delay the aging and its related diseases or to improve the diseases treatment. Therapeutic interventions towards senescent cells might allow restoring the health and curing the diseases that share basal processes, rather than curing each disease in separate and symptomatic way. Here, we review observations on ROS ability of inducing cell senescence through novel mechanisms that underpin aging processes. Particular emphasis is addressed to the novel mechanisms of ROS involvement in epigenetic regulation of cell senescence and aging, with the aim to individuate specific pathways, which might promote healthy lifespan and improve aging.

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Figures

Figure 1
Figure 1
Schematic representation of ROS signaling in physiological and pathological conditions. Low and medium ROS levels produced by mitochondria and NADPH oxidase activate cell ROS sensitive proteins and epigenetic machinery. High ROS level causes nucleic acids, lipid, and proteins damage possibly involved in accelerated aging, cell death, and age-related diseases.
Figure 2
Figure 2
ROS-mediated senescence. Besides causing DNA damage and mitochondria dysfunction, OS activates p53 that, in turn, induces prooxidant genes and imbalances antioxidant genes induction. The set of alterations caused by ROS lead to induction of cell senescence, which, in turn, can develop both positive and negative effects; miR34a expression increases with aging in many tissues downregulating SIRT1 protein activity (a longevity promoting factor) and PNUT protein (a DNA protecting factor which prevents telomere attrition and is involved in tissues repairs).
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