Mitohormesis

Jeanho Yun, Toren Finkel

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)757-766
Number of pages10
JournalCell Metabolism
Volume19
Issue number5
DOIs
StatePublished - May 6 2014
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Physiology
  • Medicine(all)

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  • Cite this

    Yun, J., & Finkel, T. (2014). Mitohormesis. Cell Metabolism, 19(5), 757-766. https://doi.org/10.1016/j.cmet.2014.01.011