Diagrammatic representation of downstream signaling driven by the mTORC1. (A) Targeting mTOR with rapamycin or knockout of raptor prevents activation of mTORC1, and therefore prevents increased mitochondrial function and reactive oxygen species production. (B) Model of mTORC1 activation. In the young, cellular redox is maintained by adequate production of the antioxidants superoxide dismutase and glutathione, and competent mitochondrial function prevents venous thromboembolism (left). During aging, the levels of superoxide dismutase and glutathione decrease, and mitochondrial function deteriorates, resulting in the accumulation of reactive oxygen species. Hyperactivation of mTORC1 by reactive oxygen species results in further oxidative stress and a vicious cycle of oxidant production. Targeting mTORC1 function or antioxidant therapy contributes to reduced risk of venous thrombosis. KO, knockout; ROS, reactive oxygen species.