Mitochondrial calcium cycling in neuronal function and neurodegeneration

Walters, Grant C.; Usachev, Yuriy M.

doi:10.3389/fcell.2023.1094356

Cited by 105Mitochondrial Function and PathologyIon channel regulation and functionIon Channels and Receptors

Mitochondrial calcium cycling in neuronal function and neurodegeneration

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Walters, Grant C., Usachev, Yuriy M.·2023·Frontiers in Cell and Developmental Biology

DOI 10.3389/fcell.2023.1094356PMC PMC9902777

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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.

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Excessive or prolonged activation of CaV channels leads to calcium overload in mitochondria, disrupting their normal function.
“excessive or prolonged activation of CaV channels leads to calcium overload in mitochondria, disrupting their normal function at multiple levels and significantly impacting cellular development and homeostasis101,102.”
From CYFIP1 governs the development of cortical axons by modulating calcium availability (2025) · cites this paper as [102]
The Figure 3 caption in the neurological-diseases section links CaV2 and CaV3 channels, alongside NMDA and AMPA receptors, to mitochondrial calcium buildup during seizures; it says long or repeated seizures can cause mitochondrial overload and neuronal toxicity (page unavailable). The mPTP section explains how overload impairs mitochondrial function. The paper does not establish that excessive or prolonged CaV activation alone causes this outcome across cells generally. (LLM, conf=0.83)
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Authors: Walters, G. C., & Usachev, Y. M.
Affiliations: University of Iowa (US)
Corresponding author: Walters, Grant C.
Usachev, Yuriy M.
ORCID: Walters, Grant C.
Usachev, Yuriy M.
Venue: Frontiers in Cell and Developmental Biology
Publisher: Frontiers Media SA
Published: 2023-01-24
Volume: 11
Pages: 1094356-1094356
ISSN: 2296-634X (ISSN-L)
DOI: 10.3389/fcell.2023.1094356
PMC: PMC9902777
OpenAlex: W4317907766
Cited by: 105
References: 336
Citations by year: 2026: 35 · 2025: 37 · 2024: 22 · 2023: 11
FWCI: 2.77
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Institutes of Health (NS125884)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords: mitochondrial calcium uniporter, mitochondrial calcium uptake, mitochondrial calcium release, calcium buffering, neuronal excitability, synaptic transmission, neurodegeneration, mitochondrial dysfunction, epilepsy, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, reactive oxygen species, apoptosis

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Mitochondrial calcium cycling in neuronal function and neurodegeneration

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