Role of Mitochondrial Reactive Oxygen Species in the Activation of Cellular Signals, Molecules, and Function.
Mitochondria are a major source of intracellular energy and reactive oxygen species in cells, but are also increasingly being recognized as a controller of cell death. Here, we review evidence of signal transduction control by mitochondrial superoxide generation via the nuclear factor-κB (NF-κB) and GATA signaling pathways. We have also reviewed the effects of ROS on the activation of MMP and HIF. There is significant evidence to support the hypothesis that mitochondrial superoxide can initiate signaling pathways following transport into the cytosol. In this study, we provide evidence of TATA signal transductions by mitochondrial superoxide. Oxidative phosphorylation via the electron transfer chain, glycolysis, and generation of superoxide from mitochondria could be important factors in regulating signal transduction, cellular homeostasis, and cell death.
Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8544, Japan. hindoh@dent.kagoshima-u.ac.jp.|Department of Space Environmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8544, Japan. hindoh@dent.kagoshima-u.ac.jp.|Graduate Center of Toxicology and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40506, USA. hindoh@dent.kagoshima-u.ac.jp.
Hiroko P
HP
Indo
The Heart Research Institute, 7 Eliza Street, Newtown, NSW, 2042, Australia. clare.hawkins@hri.org.au.|Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia. clare.hawkins@hri.org.au.
Clare L
CL
Hawkins
Quantitative RedOx Sensing Team (QRST), Department of Basic Medical Sciences for Radiation Damages, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum and Radiological Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba, 263-8555, Japan.
Ikuo
I
Nakanishi
Quantitative RedOx Sensing Team (QRST), Department of Basic Medical Sciences for Radiation Damages, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum and Radiological Science and Technology (QST), 4-9-1 Anagawa, Inage-ku, Chiba, 263-8555, Japan.
Ken-Ichiro
KI
Matsumoto
Division of Gastroenterology, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki Prefecture, 305-8575, Japan.
Hirofumi
H
Matsui
Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8544, Japan.
Shigeaki
S
Suenaga
Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Blegdamsvej 3, Copenhagen, 2200, Denmark.
Michael J
MJ
Davies
Graduate Center of Toxicology and Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, 40506, USA.
Daret K
DK
St Clair
Division of Oxidative Stress Research, Showa Pharmaceutical University, Machida, Tokyo, 194-8543, Japan.
Toshihiko
T
Ozawa
Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8544, Japan. hmajima@dent.kagoshima-u.ac.jp.|Department of Space Environmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8544, Japan. hmajima@dent.kagoshima-u.ac.jp.
Hideyuki J
HJ
Majima
D000818:Animals; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D016328:NF-kappa B / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
D016328:NF-kappa B; D017382:Reactive Oxygen Species
Activation; GATA; HIF; MMP; Mitochondria; Mitochondrial ROS; MnSOD; NF-κB; Reactive oxygen species; Signal transduction; Superoxide