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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Published in:Frontiers in cell and developmental biology Vol. 11; p. 1094356
Main Authors: Walters, Grant C., Usachev, Yuriy M.
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media SA 24.01.2023
Frontiers Media S.A
Subjects:
Alzheimer's disease
Amyotrophic lateral sclerosis
Apoptosis
calcium
Calcium (mitochondrial)
Calcium buffering
Calcium influx
Calcium signalling
Calcium transport
Cell and Developmental Biology
Dehydrogenases
Disease
Epilepsy
Excitability
Gene expression
MCU
Mitochondria
Mutation
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
neuronal calcium homeostasis
Neurotoxicity
Oxidative stress
Parkinson's disease
Permeability
Physiology
Reactive oxygen species
Synaptic transmission
neurodegeneration
calcium
mitochondria
MCU
neuronal calcium homeostasis
ISSN:2296-634X, 2296-634X
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Abstract 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.
AbstractList Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca2+) buffering, and apoptotic signaling. In neurons, Ca2+ buffering is particularly important as it helps to shape Ca2+ signals and to regulate numerous Ca2+-dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca2+ uniporter (MCU) and other molecular components of mitochondrial Ca2+ transport has provided insight into the roles that mitochondrial Ca2+ regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca2+ uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca2+-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 Ca2+ uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.
Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca ) buffering, and apoptotic signaling. In neurons, Ca buffering is particularly important as it helps to shape Ca signals and to regulate numerous Ca -dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca uniporter (MCU) and other molecular components of mitochondrial Ca transport has provided insight into the roles that mitochondrial Ca regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca -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 uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.
Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca2+) buffering, and apoptotic signaling. In neurons, Ca2+ buffering is particularly important as it helps to shape Ca2+ signals and to regulate numerous Ca2+-dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca2+ uniporter (MCU) and other molecular components of mitochondrial Ca2+ transport has provided insight into the roles that mitochondrial Ca2+ regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca2+ uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca2+-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 Ca2+ uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca2+) buffering, and apoptotic signaling. In neurons, Ca2+ buffering is particularly important as it helps to shape Ca2+ signals and to regulate numerous Ca2+-dependent functions including neuronal excitability, synaptic transmission, gene expression, and neuronal toxicity. Over the past decade, identification of the mitochondrial Ca2+ uniporter (MCU) and other molecular components of mitochondrial Ca2+ transport has provided insight into the roles that mitochondrial Ca2+ regulation plays in neuronal function in health and disease. In this review, we discuss the many roles of mitochondrial Ca2+ uptake and release mechanisms in normal neuronal function and highlight new insights into the Ca2+-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 Ca2+ uptake and release mechanisms could facilitate the development of novel therapeutic strategies for neurological diseases.
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.
Author Walters, Grant C.
Usachev, Yuriy M.
AuthorAffiliation Department of Neuroscience and Pharmacology , Iowa Neuroscience Institute , University of Iowa , Iowa City , IA , United States
AuthorAffiliation_xml – name: Department of Neuroscience and Pharmacology , Iowa Neuroscience Institute , University of Iowa , Iowa City , IA , United States
Author_xml – sequence: 1
  givenname: Grant C.
  surname: Walters
  fullname: Walters, Grant C.
– sequence: 2
  givenname: Yuriy M.
  surname: Usachev
  fullname: Usachev, Yuriy M.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36760367$$D View this record in MEDLINE/PubMed
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Keywords neurodegeneration
calcium
mitochondria
MCU
neuronal calcium homeostasis
Language English
License Copyright © 2023 Walters and Usachev.
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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
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Snippet Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca 2+ )...
Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca )...
Mitochondria are essential for proper cellular function through their critical roles in ATP synthesis, reactive oxygen species production, calcium (Ca2+)...
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SubjectTerms Alzheimer's disease
Amyotrophic lateral sclerosis
Apoptosis
calcium
Calcium (mitochondrial)
Calcium buffering
Calcium influx
Calcium signalling
Calcium transport
Cell and Developmental Biology
Dehydrogenases
Disease
Epilepsy
Excitability
Gene expression
MCU
Mitochondria
Mutation
Neurodegeneration
Neurodegenerative diseases
Neurological diseases
neuronal calcium homeostasis
Neurotoxicity
Oxidative stress
Parkinson's disease
Permeability
Physiology
Reactive oxygen species
Synaptic transmission
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Title Mitochondrial calcium cycling in neuronal function and neurodegeneration
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