Neuronal mitochondria and apoptosis signaling pathways play an important role in cell death during transient cerebral ischemia
10.3969/j.issn.2095-4344.2015.15.025
- VernacularTitle:线粒体及凋亡相关信号途径在脑缺血性损伤细胞死亡过程中的重要角色
- Author:
Haibin DAI
;
Xiaolei MIAO
;
Qing JI
;
Manlin DUAN
- Publication Type:Journal Article
- Keywords:
Subject headings：Tissue Engineering;
Mitochondria;
Apoptosis;
Brain Ischemia
- From:
Chinese Journal of Tissue Engineering Research
2015;(15):2425-2430
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Although the mechanism why neuronal cels wil die after transient cerebral ischemia has not been completely elucidated, many researches nowadays have investigated the pathological mechanism in the level of celular organs, such as mitochondria.
OBJECTIVE:To summarize and discuss the functions of neuronal mitochondria and apoptosis signaling pathways in transient cerebral ischemia.
METHODS: A computer-based online retrieval was performed to search papers in CNKI and PubMed databases using the key words of “cerebral ischemia, mitochondrion, apoptosis, reactive oxygen species, reperfusion, superoxide dismutase, nitric oxide synthase, Bcl-2 protein family, review” in Chinese and English, respectively. Papers published recently or in the prestigious journals were selected in the same field. After excluding objective-independent papers and repeated studies, 50 papers were included for further analysis.
RESULTS AND CONCLUSION:Recently mitochondria are found to play an important role after transient cerebral ischemia by producing a lot of reactive oxygen species to activate many kinds of signaling pathways and regulate mitochondria-mediated apoptosis. Reactive oxygen cannot only induce biomacromolecule injury but also induce apoptosis signal transduction. Deeply investigation is needed on the pathological mechanism after transient cerebral ischemia.
