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.

Nutritional Strategies and Aging: Current Evidence and Future Directions

Castelli, Serena;Aiello, Gilda;Massimino, Elena;Lombardo, Mauro;Tripodi, Gianluca;Baldelli, Sara
2026-01-01

Abstract

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.
2026
aging
oxidative stress
nutrition-based interventions
nutraceuticals
mitochondrial health
disease prevention
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12078/33266
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact