Mitochondrial stress induces cellular senescence in an mTORC1-dependent manner
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文摘

Low level ROS leads to mTORC1 activation, high levels of ROS inhibit mTORC1 through AMPK.

mTORC1/S6 kinase activity can target HDM2 following mitochondrial dysfunction to activate p53.

Changes in mTORC1 activity alter oxygen consumption rates and are tied to energy status.

Elevated mTORC1 activity may represent a chronic stress response leading to senescence.

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