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Aberrant mTOR activation in senescence and aging: A mitochondrial stress response?
Journal article   Open access   Peer reviewed

Aberrant mTOR activation in senescence and aging: A mitochondrial stress response?

Timothy Nacarelli, Ashley Azar and Christian Sell
Experimental gerontology, v 68
Aug 2015
PMID: 25449851
url
https://europepmc.org/articles/pmc4589173View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Aging - physiology Animals Autophagy - physiology Cellular Senescence - physiology Humans Longevity - physiology Mechanistic Target of Rapamycin Complex 1 Mice Mitochondria - metabolism Multiprotein Complexes - metabolism Reactive Oxygen Species - metabolism Signal Transduction - physiology Stress, Physiological - physiology TOR Serine-Threonine Kinases - metabolism
Unexpected activation of mTOR signaling, measured by ribosomal S6 phosphorylation or ribosomal S6 kinase (p70S6K) activity, has been reported in aging-related settings. Evidence of elevated mTOR activity has been reported in the heart and muscle tissue in aged mice and humans, mouse models of progeria, and senescent human fibroblasts. We explore these reports and the possibility that activation of the mTOR/p70S6K kinase pathway may represent a ROS-mediated response to mitochondrial stress leading to the activation of senescence. This activation is a hallmark of both aged tissue and senescent human cells.

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Web of Science research areas
Geriatrics & Gerontology
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