Abstract：
:For many years, mitochondria were viewed as semiautonomous organelles, required only for cellular energetics. This view has been largely supplanted by the concept that mitochondria are fully integrated into the cell and that mitochondrial stresses rapidly activate cytosolic signaling pathways that ultimately alter nuclear gene expression. Remarkably, this coordinated response to mild mitochondrial stress appears to leave the cell less susceptible to subsequent perturbations. This response, termed mitohormesis, is being rapidly dissected in many model organisms. A fuller understanding of mitohormesis promises to provide insight into our susceptibility for disease and potentially provide a unifying hypothesis for why we age.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Yun J,Finkel Tdoi
10.1016/j.cmet.2014.01.011subject
Has Abstractpub_date
2014-05-06 00:00:00pages
757-66issue
5eissn
1550-4131issn
1932-7420pii
S1550-4131(14)00017-5journal_volume
19pub_type
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