Mitochondrial stress: Balancing friend and foe

作者:Runkel Eva Diana; Baumeister Ralf; Schulze Ekkehard*
来源:Experimental Gerontology, 2014, 56: 194-201.
DOI:10.1016/j.exger.2014.02.013

摘要

Mitochondria are vital organelles of the aerobic eukaryotic cell. Their dysfunction associates with aging and wide-spread age-related diseases. To sustain mitochondrial integrity, the cell executes a distinct set of stress-induced protective responses. The mitochondrial unfolded protein response (UPRmt) is a response of the cell to mitochondrial damage. The transcription factor ATFS-1 triggers UPRmt 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, UPRmt 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 UPRmt, 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.

  • 出版日期2014-8