Mitochondrial Ca2+ in neurodegenerative disorders

R Abeti, AY Abramov - Pharmacological research, 2015 - Elsevier
R Abeti, AY Abramov
Pharmacological research, 2015Elsevier
Functional mitochondria are vital to accomplish their key role in the cell, by maintaining the
energy metabolism, buffering of the Ca 2+ signal and directing the cell death mechanism.
Mitochondrial Ca 2+ can stimulate ATP production or trigger the opening of mitochondrial
permeability transition pore and activating the cell death cascade. Mitochondrial Ca 2+
uptake play a crucial role in neurons by buffering excessive Ca 2+ from the cytosol at the
time of the transmission of the signal. Changes in the maintenance of mitochondrial Ca 2+ …
Abstract
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.
Elsevier