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Cell. 2015 Oct 22;163(3):560-9. doi: 10.1016/j.cell.2015.10.001. Epub 2015 Oct 22.

Mitochondrial ROS signaling in organismal homeostasis.

Author information

1
Department of Pathology, Yale School of Medicine, New Haven CT 06520; Department of Genetics, Yale School of Medicine, New Haven CT 06520; Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale School of Medicine, New Haven CT 06520. Electronic address: gerald.shadel@yale.edu.
2
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale School of Medicine, New Haven CT 06520; Section of Comparative Medicine, Yale School of Medicine, New Haven CT 06520; Department of Neurobiology, Yale School of Medicine, New Haven CT 06520. Electronic address: tamas.horvath@yale.edu.

Abstract

Generation, transformation, and utilization of organic molecules in support of cellular differentiation, growth, and maintenance are basic tenets that define life. In eukaryotes, mitochondrial oxygen consumption plays a central role in these processes. During the process of oxidative phosphorylation, mitochondria utilize oxygen to generate ATP from organic fuel molecules but in the process also produce reactive oxygen species (ROS). While ROS have long been appreciated for their damage-promoting, detrimental effects, there is now a greater understanding of their roles as signaling molecules. Here, we review mitochondrial ROS-mediated signaling pathways with an emphasis on how they are involved in various basal and adaptive physiological responses that control organismal homeostasis.

PMID:
26496603
PMCID:
PMC4634671
DOI:
10.1016/j.cell.2015.10.001
[Indexed for MEDLINE]
Free PMC Article

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