title: Mitohormesis.
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.
authors.affiliation: Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA; Department of Biochemistry and Mitochondria Hub Regulation Center, College of Medicine, Dong-A University, Busan 602-714, South Korea.
authors.forename: Jeanho
authors.initials: J
authors.lastname: Yun
authors.affiliation: Center for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA. Electronic address: finkelt@nih.gov.
authors.forename: Toren
authors.initials: T
authors.lastname: Finkel
mesh_terms: D000818:Animals; D015870:Gene Expression / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D013312:Stress, Physiological / Q000502:physiology