Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia

作者：Niizuma Kuniyasu; Yoshioka Hideyuki; Chen Hai; Kim Gab Seok; Jung Joo Eun; Katsu Masataka; Okami Nobuya; Chan Pak H^*

来源：Biochimica et Biophysica Acta-Molecular Basis of Disease, 2010, 1802(1): 92-99.

DOI：10.1016/j.bbadis.2009.09.002

• Mitochondria
• Cerebral ischemia
• SOD1
• Reactive oxygen species
• Neuronal death
• PIDD

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.

• 出版日期2010-1