Davalli Pierpaola, Mitic Tijana, Caporali Andrea, Lauriola Angela, D'Arca Domenico
Department of Biomedical, Metabolic and Neural Sciences, University of Modena & Reggio Emilia, 41125 Modena, Italy.
Bristol Heart Institute, University of Bristol, Bristol BS2 8HW, UK.
Oxid Med Cell Longev. 2016;2016:3565127. doi: 10.1155/2016/3565127. Epub 2016 May 10.
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.
衰老过程会在多个层面上使人体功能恶化,从而导致其抵抗压力、损伤和疾病的能力逐渐下降。除了基因表达和代谢控制的变化外,衰老速率还与高水平活性氧(ROS)和/或活性氮(RNS)的产生有关。ROS水平的特定升高已被证明对细胞衰老过程的诱导和维持具有潜在的关键作用。人们对ROS、衰老、与年龄相关的病理以及细胞衰老之间的因果关系进行了深入研究。衰老细胞已被提议作为延缓衰老及其相关疾病或改善疾病治疗的干预靶点。针对衰老细胞的治疗干预可能会恢复健康并治愈具有共同基础过程的疾病,而不是以单独和对症的方式治疗每种疾病。在此,我们回顾了关于ROS通过支撑衰老过程的新机制诱导细胞衰老能力的观察结果。特别强调了ROS参与细胞衰老和衰老表观遗传调控的新机制,旨在确定可能促进健康寿命和改善衰老的特定途径。