The activation of mTORC1 by growth factors and nutrients inhibits autophagy and promotes protein synthesis. Over time, this may promote cellular stress (protein aggregation, organelle dysfunction, oxidative stress), which might lead to damage accumulation, a reduction in cell function and thus promote the development of aging-related diseases. Also, mTORC1 activation induces stem cell exhaustion, which reduces tissue repair and promotes tissue dysfunction. Dietary restriction and rapamycin may delay aging and increase longevity by regulating these processes downstream of mTORC1.