Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia.
Mitochondria play important roles as the powerhouse of the cell. After cerebral ischemia, mitochondria overproduce reactive oxygen species (ROS), which have been thoroughly studied with the use of superoxide dismutase transgenic or knockout animals. ROS directly damage lipids, proteins, and nucleic acids in the cell. Moreover, ROS activate various molecular signaling pathways. Apoptosis-related signals return to mitochondria, then mitochondria induce cell death through the release of pro-apoptotic proteins such as cytochrome c or apoptosis-inducing factor. Although the mechanisms of cell death after cerebral ischemia remain unclear, mitochondria obviously play a role by activating signaling pathways through ROS production and by regulating mitochondria-dependent apoptosis pathways.
Niizuma
Kuniyasu
K
Department of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USA.
Yoshioka
Hideyuki
H
Chen
Hai
H
Kim
Gab Seok
GS
Jung
Joo Eun
JE
Katsu
Masataka
M
Okami
Nobuya
N
Chan
Pak H
PH
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002545:Brain Ischemia / Q000378:metabolism*; D016923:Cell Death; D006801:Humans; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D009474:Neurons / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction
D017382:Reactive Oxygen Species