mTOR is a key regulator of aging and age-related diseases. It is a serine/threonine protein kinase in the PI(3)K-related family that controls cellular growth and metabolism in response to nutrients and hormones. mTOR functions in two complexes, mTORC1 and mTORC2. mTORC1 is inhibited by rapamycin, which extends lifespan in various organisms, including yeast, nematodes, fruitflies, and mice. mTORC1 is activated by insulin and other growth factors, and repressed by AMPK. It promotes protein synthesis, lipid biosynthesis, and autophagy, while repressing degradation. mTORC1 also regulates glucose metabolism and mitochondrial function through HIF-1α and PGC-1α. mTOR is involved in longevity pathways, including dietary restriction and insulin/IGF-1-like signaling. Dietary restriction reduces mTORC1 activity and extends lifespan. mTORC1 inhibition is linked to reduced mRNA translation and increased autophagy, which may contribute to longevity. mTORC1 also interacts with the hypoxic response, which is involved in aging. mTORC1 inhibition has been shown to extend lifespan in yeast, nematodes, fruitflies, and mice, and may have similar effects in humans. mTOR is also involved in stress resistance, mitochondrial function, inflammation, and stem cell function. mTORC1 inhibition can improve cognitive function and reduce the risk of age-related diseases. However, mTOR inhibitors like rapamycin have potential side effects, including hyperlipidaemia and hyperglycaemia. Despite these challenges, mTOR inhibitors show promise in delaying aging and reducing age-related pathologies. Future research aims to better understand the mechanisms of mTOR regulation and its potential therapeutic applications in aging and age-related diseases.mTOR is a key regulator of aging and age-related diseases. It is a serine/threonine protein kinase in the PI(3)K-related family that controls cellular growth and metabolism in response to nutrients and hormones. mTOR functions in two complexes, mTORC1 and mTORC2. mTORC1 is inhibited by rapamycin, which extends lifespan in various organisms, including yeast, nematodes, fruitflies, and mice. mTORC1 is activated by insulin and other growth factors, and repressed by AMPK. It promotes protein synthesis, lipid biosynthesis, and autophagy, while repressing degradation. mTORC1 also regulates glucose metabolism and mitochondrial function through HIF-1α and PGC-1α. mTOR is involved in longevity pathways, including dietary restriction and insulin/IGF-1-like signaling. Dietary restriction reduces mTORC1 activity and extends lifespan. mTORC1 inhibition is linked to reduced mRNA translation and increased autophagy, which may contribute to longevity. mTORC1 also interacts with the hypoxic response, which is involved in aging. mTORC1 inhibition has been shown to extend lifespan in yeast, nematodes, fruitflies, and mice, and may have similar effects in humans. mTOR is also involved in stress resistance, mitochondrial function, inflammation, and stem cell function. mTORC1 inhibition can improve cognitive function and reduce the risk of age-related diseases. However, mTOR inhibitors like rapamycin have potential side effects, including hyperlipidaemia and hyperglycaemia. Despite these challenges, mTOR inhibitors show promise in delaying aging and reducing age-related pathologies. Future research aims to better understand the mechanisms of mTOR regulation and its potential therapeutic applications in aging and age-related diseases.