Mitochondrial Ca2+ in neurodegenerative disorders

被引:87
作者
Abeti, Rosella [1 ]
Abramov, Andrey Y. [1 ]
机构
[1] UCL Inst Neurol, Dept Mol Neurosci, London, England
关键词
Mitochondria; Calcium; Neurodegeneration; Neurons; Astrocyte; Alzheimer's disease; Parkinson's disease; PERMEABILITY TRANSITION PORE; PINK1-ASSOCIATED PARKINSONS-DISEASE; HUNTINGTON-DISEASE; CALCIUM HOMEOSTASIS; ALZHEIMERS-DISEASE; CELL-DEATH; INTRACELLULAR CALCIUM; ESSENTIAL COMPONENT; HEART-MITOCHONDRIA; NA+/CA2+ EXCHANGE;
D O I
10.1016/j.phrs.2015.05.007
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Functional mitochondria are vital to accomplish their key role in the cell, by maintaining the energy metabolism, buffering of the Ca2+ signal and directing the cell death mechanism. Mitochondrial Ca2+ can stimulate ATP production or trigger the opening of mitochondrial permeability transition pore and activating the cell death cascade. Mitochondrial Ca2+ uptake play a crucial role in neurons by buffering excessive Ca2+ from the cytosol at the time of the transmission of the signal. Changes in the maintenance of mitochondrial Ca2+ may trigger neuronal cell death. Abnormality in mitochondrial Ca2+ handling has been detected in a range of neurodegenerative diseases, and emerging evidence from disease models suggests that mitochondrial Ca2+ may play a role in disease pathogenesis. In this review, we assess how mitochondrial Ca2+ imbalance may be a trigger in common neurodegenerative disease. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:377 / 381
页数:5
相关论文
共 78 条
[1]
β-amyloid activates PARP causing astrocytic metabolic failure and neuronal death [J].
Abeti, Rosella ;
Abramov, Andrey Y. ;
Duchen, Michael R. .
BRAIN, 2011, 134 :1658-1672
[2]
Abramov A. Y., 2014, BIOCH SOC T, V42
[3]
Mechanisms underlying the loss of mitochondrial membrane potential in glutamate excitotoxicity [J].
Abramov, Andrey Y. ;
Duchen, Michael R. .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2008, 1777 (7-8) :953-964
[4]
Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell death [J].
Abramov, Andrey Y. ;
Fraley, Cresson ;
Diao, Catherine T. ;
Winkfein, Robert ;
Colicos, Michael A. ;
Duchen, Michael R. ;
French, Robert J. ;
Pavlov, Evgeny .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (46) :18091-18096
[5]
Membrane cholesterol content plays a key role in the neurotoxicity of β-amyloid: implications for Alzheimer's disease [J].
Abramov, Andrey Y. ;
Ionov, Maksim ;
Pavlov, Evgeny ;
Duchen, Michael R. .
AGING CELL, 2011, 10 (04) :595-603
[6]
Bioenergetic Consequences of PINK1 Mutations in Parkinson Disease [J].
Abramov, Andrey Yurevich ;
Gegg, Matthew ;
Grunewald, Anne ;
Wood, Nicholas William ;
Klein, Christine ;
Schapira, Anthony Henry Vernon .
PLOS ONE, 2011, 6 (10)
[7]
The role of an astrocytic NADPH oxidase in the neurotoxicity of amyloid beta peptides [J].
Abramov, AY ;
Duchen, MR .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2005, 360 (1464) :2309-2314
[8]
Calcium signals induced by amylold β peptide and their consequences in neurons and astrocytes in culture [J].
Abramov, AY ;
Canevari, L ;
Duchen, MR .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2004, 1742 (1-3) :81-87
[9]
β-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase [J].
Abramov, AY ;
Canevari, L ;
Duchen, MR .
JOURNAL OF NEUROSCIENCE, 2004, 24 (02) :565-575
[10]
Abramov AY, 2003, J NEUROSCI, V23, P5088