Cellular autophagy and aging: role in intermittent fasting-induced health benefits

Autophagy, an evolutionarily conserved cellular process, is essential for maintaining homeostasis by regulating the turnover and function of organelles and proteins. It is constitutively active at the basal level in most cell types, ensuring cellular health through the degradation and recycling of intracellular components. As we age, the decline in autophagic activity leads to the accumulation of damaged organelles and proteins, which contribute to the development of age-related diseases, such as neurodegenerative disorders, cardiovascular diseases, and cancer. Intermittent fasting (IF) has emerged as a potent inducer of autophagy, primarily through the inhibition of the mechanistic target of rapamycin (mTOR) pathway. This induction not only facilitates the clearance of cellular debris but also provides essential substrates for cellular repair and regeneration, thereby promoting overall cellular health and longevity. This chapter delves into the molecular mechanisms involved in autophagy, focusing on key regulatory proteins like mTOR, AMP-activated protein kinase, and unc-51-like autophagy-activating kinase 1, and explores how their dysregulation during aging accelerates the aging process. By enhancing the autophagic activity, IF has the potential to counteract aging, reduce oxidative stress, and improve metabolic health, thereby lowering the risk of age-related diseases. Based on a comprehensive review of current scientific literature, this chapter suggests IF as a therapeutic strategy to boost autophagy and promote healthy aging.