The Function of the Mitochondrial Calcium Uniporter in Neurodegenerative Disorders

被引：57
作者：
Liao, Yajin [1 ,2 ]
Dong, Yuan [3 ]
Cheng, Jinbo [2 ]
机构：
[1] Beijing Inst Basic Med Sci, Brain Sci Ctr, 27 Taiping Rd, Beijing 100039, Peoples R China
[2] Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China
[3] Qingdao Univ, Dept Biochem, Coll Med, Qingdao 266071, Peoples R China
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2017年 / 18卷 / 02期
关键词：
MCU; neurodegenerative disorder; inflammation; iron overload; oxidative stress; METABOTROPIC GLUTAMATE-RECEPTOR; CEREBRAL-ARTERY OCCLUSION; RAT-LIVER MITOCHONDRIA; CYTOSOLIC-FREE CALCIUM; PROGRAMMED CELL-DEATH; ACUTE ISCHEMIC-STROKE; OXIDATIVE STRESS; ESSENTIAL COMPONENT; PARKINSON DISEASE; IRON ACCUMULATION;
D O I：
10.3390/ijms18020248
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The mitochondrial calcium uniporter (MCU)a calcium uniporter on the inner membrane of mitochondriacontrols the mitochondrial calcium uptake in normal and abnormal situations. Mitochondrial calcium is essential for the production of adenosine triphosphate (ATP); however, excessive calcium will induce mitochondrial dysfunction. Calcium homeostasis disruption and mitochondrial dysfunction is observed in many neurodegenerative disorders. However, the role and regulatory mechanism of the MCU in the development of these diseases are obscure. In this review, we summarize the role of the MCU in controlling oxidative stress-elevated mitochondrial calcium and its function in neurodegenerative disorders. Inhibition of the MCU signaling pathway might be a new target for the treatment of neurodegenerative disorders.
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页数：16
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