Journal
MITOCHONDRION
Volume 11, Issue 3, Pages 369-381Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2011.01.010
Keywords
Aging; Apoptosis; Cardiolipin; Cell signaling; Cytochrome c; Oxidative phosphorylation; Reactive oxygen species
Categories
Funding
- National Institutes of Health [GM089900, HL70755, HL094488, U19A1068021, OH008282]
- Center for Molecular Medicine and Genetics
- Cardiovascular Research Institute, Wayne State University School of Medicine, Detroit
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Cytochrome c (Cytc) is essential in mitochondrial electron transport and intrinsic type II apoptosis. Mammalian Cytc also scavenges reactive oxygen species (ROS) under healthy conditions, produces ROS with the co-factor p66(Shc), and oxidizes cardiolipin during apoptosis. The recent finding that Cytc is phosphorylated in vivo underpins a model for the pivotal role of Cytc regulation in making life and death decisions. An apoptotic sequence of events is proposed involving changes in Cytc phosphorylation, increased ROS via increased mitochondrial membrane potentials or the p66(Shc) pathway, and oxidation of cardiolipin by Cytc followed by its release from the mitochondria. Cytc regulation in respiration and cell death is discussed in a human disease context including neurodegenerative and cardiovascular diseases, cancer, and sepsis. (C) 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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