Mitochondrial stress: balancing friend and foe.

Autor: Runkel ED; Faculty of Biology, Institute of Biology III, Germany; BIOSS Centre for Biological Signalling Studies, Germany; Spemann Graduate School of Biology and Medicine, Germany., Baumeister R; Faculty of Biology, Institute of Biology III, Germany; Faculty of Medicine, ZBMZ Center of Biochemistry and Molecular Cell Research, Germany; BIOSS Centre for Biological Signalling Studies, Germany; Spemann Graduate School of Biology and Medicine, Germany., Schulze E; Faculty of Biology, Institute of Biology III, Germany; BIOSS Centre for Biological Signalling Studies, Germany. Electronic address: ekkehard.schulze@biologie.uni-freiburg.de.
Jazyk: angličtina
Zdroj: Experimental gerontology [Exp Gerontol] 2014 Aug; Vol. 56, pp. 194-201. Date of Electronic Publication: 2014 Mar 03.
DOI: 10.1016/j.exger.2014.02.013
Abstrakt: Mitochondria are vital organelles of the aerobic eukaryotic cell. Their dysfunction associates with aging and widespread age-related diseases. To sustain mitochondrial integrity, the cell executes a distinct set of stress-induced protective responses. The mitochondrial unfolded protein response (UPR(mt)) is a response of the cell to mitochondrial damage. The transcription factor ATFS-1 triggers UPR(mt) effector gene expression in the nucleus. The selective exclusion of ATFS-1 from mitochondrial import by stress-induced alterations of the mitochondrial membrane potential is currently discussed as key activation mechanism. Surprisingly, UPR(mt) activation often coincides with a lifespan extension in Caenorhabditis elegans and the same has recently been reported for mammalian cells. This review summarizes the current model of the UPR(mt), its inducers, and its crosstalk with other cellular stress responses. It focuses on the role of mitochondrial function as a regulator of aging and longevity.
(Copyright © 2014 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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