Journal of Capital Medical University ›› 2013, Vol. 34 ›› Issue (1): 75-79.doi: 10.3969/j.issn.1006-7795.2013.01.014

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Recent progress in studies on the role of Zn2+ in cerebral ischemia

LI Sen, LIU Kejian, ZHAO Yongmei   

  1. Xuanwu Hospital, Capital Medical University, Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing Geriatric Medical Research Center, Beijing 100053, China
  • Received:2012-10-09 Online:2013-02-21 Published:2013-02-25
  • Supported by:

    This study was supported by National Natural Science Foundation of China (81171242),Natural Science Foundation of Beijing (7122036),Public Foundation of Beijing Brain Diseases Key Laboratory(2012NZDJ03).

Abstract:

Recent reports have indicated that zinc ion (Zn2+) plays an important role in the mechanism of brain injury following cerebral ischemia. Large amount of Zn2+ is released from synaptic vesicles and accumulates in postsynaptic neurons following cerebral ischemia. In addition, oxidative stress and acidosis, both of which occur prominently in ischemia, can induce Zn2+ release from zinc-ligands such as metallothionein proteins. Intense cytosolic Zn2+ overloads can promote pronounced mitochondrial dysfunction and reactive oxygen species generation to trigger necrosis, whereas milder cytosolic Zn2+ loads may augment apoptotic pathways. Further investigation of the contribution of Zn2+ to the mechanism of brain injury following cerebral ischemia will likely provide new preventive and therapeutic strategies for ischemic stroke.

Key words: Zn2+, cerebral ischemia, brain injury

CLC Number: