Mitochondrial calcium cycling in neuronal function and neurodegeneration

Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca 2+ ) buffering, and apoptotic signaling. In neurons, Ca 2+ buffering is particularly important as it helps to shape Ca 2+ signals and to regulate num...

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Veröffentlicht in:Frontiers in cell and developmental biology Jg. 11; S. 1094356
Hauptverfasser: Walters, Grant C., Usachev, Yuriy M.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media SA 24.01.2023
Frontiers Media S.A
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ISSN:2296-634X, 2296-634X
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Zusammenfassung:Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca 2+ ) buffering, and apoptotic signaling. In neurons, Ca 2+ buffering is particularly important as it helps to shape Ca 2+ signals and to regulate numerous Ca 2+ -dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca 2+ uniporter (MCU) and other molecular components of mitochondrial Ca 2+ transport has provided insight into the roles that mitochondrial Ca 2+ regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca 2+ uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca 2+ -dependent mechanisms that drive mitochondrial dysfunction in neurologic diseases including epilepsy, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. We also consider how targeting Ca 2+ uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.
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Reviewed by: Cecilia Hidalgo, University of Chile, Chile
Edited by: Karthik Babu Mallilankaraman, National University of Singapore, Singapore
Evgeny V. Pavlov, New York University, United States
This article was submitted to Molecular and Cellular Pathology, a section of the journal Frontiers in Cell and Developmental Biology
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2023.1094356