Mitochondrial Proteostasis in the Control of Aging and Longevity

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Mitochondrial Proteostasis in the Control of Aging and Longevity Martin Borch Jensen, Heinrich Jasper  Cell Metabolism  Volume 20, Issue 2, Pages 214-225 (August 2014) DOI: 10.1016/j.cmet.2014.05.006 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 UPRmt Signal Transduction Current model for UPRmt signal transduction based on studies in worms and mammalian cells. Signaling components identified in worms are shaded blue, and signaling components identified in mammalian cells are shaded green. See text for details. Cell Metabolism 2014 20, 214-225DOI: (10.1016/j.cmet.2014.05.006) Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 2 Cellular and Systemic Outcomes of UPRmt Activation Cell autonomous interactions between the UPRmt and processes ensuring cellular homeostasis, as well as nonautonomous interactions between local UPRmt activation and peripheral cells are depicted. Individual interactions have been identified in different model systems, and detailed characterization of these interactions is needed to obtain a comprehensive model for UPRmt responses in specific systems/tissues. See text for details. Cell Metabolism 2014 20, 214-225DOI: (10.1016/j.cmet.2014.05.006) Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 3 Integration of the UPRmt with Processes Influencing Lifespan The UPRmt intersects with most processes influencing lifespan known to date, suggesting that interventions that preserve mitochondrial function or that trigger mitoprotective responses are promising candidates for therapies extending lifespan. Cell Metabolism 2014 20, 214-225DOI: (10.1016/j.cmet.2014.05.006) Copyright © 2014 Elsevier Inc. Terms and Conditions