Interaction of Mitochondrial Calcium and ROS in Neurodegeneration

Artyom Y Baev, Andrey Y Vinokurov, Irina N Novikova, Viktor V Dremin, Elena V Potapova, Andrey Y Abramov

Research output: Contribution to journalReview articlepeer-review


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 Ca 2+ 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 Ca 2+ in brain mitochondria in physiology and beyond, considering how changes in mitochondrial metabolism or redox signaling can convert this interaction into a pathological event.

Original languageEnglish
Article number706
Issue number4
Publication statusPublished - 17 Feb 2022

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© 2022 by the authors.
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  • reactive oxygen species
  • mitochondria
  • calcium
  • neuron
  • cell death
  • permeability transition pore
  • neurodegeneration


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