Researchers: Carey E Lyons, Maria Razzoli, Alessandro Bartolomucci
Chronic stress is a risk factor for numerous aging-related diseases and has been shown to shorten lifespan in humans and other social mammals. Yet how life stress causes such a vast range of diseases is still largely unclear. In recent years, the impact of stress on health and aging has been increasingly associated with the dysregulation of the so-called hallmarks of aging. These are basic biological mechanisms that influence intrinsic cellular functions and whose alteration can lead to accelerated aging. Here, we review correlational and experimental literature (primarily focusing on evidence from humans and murine models) on the contribution of life stress - particularly stress derived from adverse social environments - to trigger hallmarks of aging, including cellular senescence, sterile inflammation, telomere shortening, production of reactive oxygen species, DNA damage, and epigenetic changes. We also evaluate the validity of stress-induced senescence and accelerated aging as an etiopathological proposition. Finally, we highlight current gaps of knowledge and future directions for the field, and discuss perspectives for translational geroscience.
References
- Cellular senescence and senolytics: the path to the clinic.
- Energetic interventions for healthspan and resiliency with aging.
- The hallmarks of aging.
- Contextual modifiers of healthspan, lifespan, and epigenome in mice under chronic social stress.
- Effect of long-term caloric restriction on DNA methylation measures of biological aging in healthy adults from the CALERIE trial.
- Loss of epigenetic information as a cause of mammalian aging.
Topic: telomeres (Graph Available)