Background: Cell senescence constitutes a critical process to respond to a variety of insults and adverse
circumstances. Senescence involves the detention of DNA replication and cell proliferation, and hence,
genetic programs associated with DNA damage response, chromosome stability, chromatin rearrangement, epigenetic
reprogramming, and cell cycle are tightly linked to the senescent phenotype. Although senescence increases
with age, the real implication of senescence regulation in the progress of aging in humans is largely discussed. In
this context, reactive oxygen species (ROS) accumulation has also been postulated to play a critical role in cell
homeostasis, aging processes, and control of proliferation.
Methods: The previous years have produced a high increase in data that refine our understanding of the role of
ROS, and their relationship with epigenetic events, in determining cellular fate.
Results: The accumulating evidence regarding the epigenetic regulation of ROS-mediated processes provides
promising tools to deepen in our comprehension of the process of senescence, and to develop novel therapeutic
strategies. In this review, we aim to provide an overview of the relationships between oxidative stress and cell
Conclusion: We provide information about the role of epigenetic regulation in senescence and aging, collecting
recent data from some examples of progeroid syndromes in which cell senescence, oxidative stress and epigenetic
mechanisms are severely impaired. Finally, a collection of data is presented regarding current pharmacological
approaches that either target or use oxidative stress-related factors or epigenetic regulators as strategies for disease