TY  - JOUR
N2  - Neurodegenerative disorders are currently incurable devastating diseases which are characterized by the slow and progressive loss of neurons in specific brain regions. Progress in the investigation of the mechanisms of these disorders helped to identify a number of genes associated with familial forms of these diseases and a number of toxins and risk factors which trigger sporadic and toxic forms of these diseases. Recently, some similarities in the mechanisms of neurodegenerative diseases were identified, including the involvement of mitochondria, oxidative stress, and the abnormality of Ca2+ signaling in neurons and astrocytes. Thus, mitochondria produce reactive oxygen species during metabolism which play a further role in redox signaling, but this may also act as an additional trigger for abnormal mitochondrial calcium handling, resulting in mitochondrial calcium overload. Combinations of these factors can be the trigger of neuronal cell death in some pathologies. Here, we review the latest literature on the crosstalk of reactive oxygen species and Ca2+ in brain mitochondria in physiology and beyond, considering how changes in mitochondrial metabolism or redox signaling can convert this interaction into a pathological event.
VL  - 11
KW  - neurodegeneration; mitochondria; calcium; reactive oxygen species; cell death; permeability transition pore; neuron
UR  - https://doi.org/10.3390/cells11040706
A1  - Baev, Artyom Y
A1  - Vinokurov, Andrey Y
A1  - Novikova, Irina N
A1  - Dremin, Viktor V
A1  - Potapova, Elena V
A1  - Abramov, Andrey Y
AV  - public
N1  - This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ID  - discovery10144432
Y1  - 2022/02/17/
PB  - MDPI AG
TI  - Interaction of Mitochondrial Calcium and ROS in Neurodegeneration
IS  - 4
JF  - Cells
ER  -