Abstract

Spermidine, a natural polyamine, has been noticed for its anti-aging properties. Supplementation of this drug prolongs lifespan and diminishes the incidence of age-related pathology. In the human population, spermidine levels decrease as aging progresses, and a potential link between diminished endogenous spermidine levels and age-related declination has been studied. At the cellular level, autophagy is the prime mode of action of spermidine known to decline with the progress of aging, similarly contributing to the accretion of impaired macromolecules and organelles through aging. Epidemiological statistics support the concept, suggesting that elevated uptake of polyamine delays aging. Here, we overview the effect of autophagy on cellular processes and age-associated diseases, emphasizing the importance of these events to the hallmarks of aging. There are numerous factors like shortening telomere, oxidative stress, mitochondrial damage, and impaired intracellular calcium signaling, which are influenced by the aging process. We hypothesize that spermidine supplements in the diet increase the telomere length. The proposed hypothesis also brings to light the differentially regulated genes involved in telomere maintenance and aging after spermidine treatment. Knowing the role of spermidine in telomere maintenance would help us understand the molecular mechanism of spermidine's effect on aging.