Aging is a progressive degenerative process characterized by the depletion of tissue stem cell reserves, organ atrophy, sarcopenia, and an impaired capacity to respond to physiological stress and injury. These changes lead to a reduction in both overall life expectancy and disease-free lifespan. Since aging represents a major risk factor for numerous diseases, including neurodegenerative, cardiovascular, and metabolic disorders, recent research has increasingly focused on identifying effective intervention strategies to promote “healthy aging” by slowing down the aging process as much as possible. At the molecular level, multiple factors contribute to cellular aging and, consequently, to the onset of senescence. These include mitochondrial dysfunction, defective DNA repair mechanisms, epigenetic reprogramming, and chronic low-grade inflammation. Among the mechanisms driving cellular senescence, oxidative stress is recognized as a key contributor to the loss of replicative capacity. When reactive oxygen species (ROS) levels exceed a critical threshold, they can damage essential macromolecules, including DNA. Therefore, ROS and oxidative stress represent crucial therapeutic targets to be considered in strategies aimed at counteracting cellular senescence. Based on these causal factors, several strategies have been identified that target modifiable lifestyle determinants, with a primary focus on nutrition and nutraceutical interventions. In this context, the present review aims to critically analyze scientific evidence regarding nutritional approaches designed to slow down the aging process, including their effects at the molecular level. Specifically, these strategies aim to reduce inflammation, preserve mitochondrial function to modulate ROS production, and protect macromolecules from oxidative stress.
Castelli et al. (Tue,) studied this question.