Cited by 2,575Mitochondrial Function and PathologyCell death mechanisms and regulationAutophagy in Disease and Therapy

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Calcium, ATP, and ROS: a mitochondrial love-hate triangle

Brookes, Paul S., Yoon, Yisang, Robotham, James L., Anders, M. W., Sheu, Shey-Shing·2004·American Journal of Physiology-Cell Physiology

DOI 10.1152/ajpcell.00139.2004

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Abstract

The mitochondrion is at the core of cellular energy metabolism, being the site of most ATP generation. Calcium is a key regulator of mitochondrial function and acts at several levels within the organelle to stimulate ATP synthesis. However, the dysregulation of mitochondrial Ca(2+) homeostasis is now recognized to play a key role in several pathologies. For example, mitochondrial matrix Ca(2+) overload can lead to enhanced generation of reactive oxygen species, triggering of the permeability transition pore, and cytochrome c release, leading to apoptosis. Despite progress regarding the independent roles of both Ca(2+) and mitochondrial dysfunction in disease, the molecular mechanisms by which Ca(2+) can elicit mitochondrial dysfunction remain elusive. This review highlights the delicate balance between the positive and negative effects of Ca(2+) and the signaling events that perturb this balance. Overall, a "two-hit" hypothesis is developed, in which Ca(2+) plus another pathological stimulus can bring about mitochondrial dysfunction.

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Authors: Brookes, P. S., Yoon, Y., Robotham, J. L., Anders, M. W., & Sheu, S.-S.
Affiliations: University of Rochester Medicine (US)
ORCID: Brookes, Paul S.
Yoon, Yisang
Sheu, Shey-Shing
Venue: American Journal of Physiology-Cell Physiology
Publisher: American Physiological Society
Published: 2004-10
Volume: 287
Issue: 4
Pages: C817-C833
ISSN: 0363-6143 (ISSN-L)
1522-1563
DOI: 10.1152/ajpcell.00139.2004
OpenAlex: W2068048197
Cited by: 2,575
References: 227
Citations by year: 2026: 72 · 2025: 112 · 2024: 126 · 2023: 138 · 2022: 144 · 2021: 177 · 2020: 162 · 2019: 134 · 2018: 125 · 2017: 125 · 2016: 122 · 2015: 125 · 2014: 124 · 2013: 129 · 2012: 124
FWCI: 5.61
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Cell Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: Medical Center, University of Rochester
National Heart, Lung, and Blood Institute (HL 33333, R01HL033333, HL-71158-01, R01HL071158)
National Institute of Diabetes and Digestive and Kidney Diseases (DK-061991, R01DK061991)
National Institute of Neurological Disorders and Stroke (NS-37710, R01NS037710)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: mitochondrial calcium homeostasis, ATP production, reactive oxygen species, mitochondrial dysfunction, mitochondrial permeability transition pore, cytochrome c release, apoptosis, two-hit hypothesis, mitochondrial bioenergetics, calcium signaling
MeSH terms: Adenosine Triphosphate, Calcium, Energy Metabolism, Ion Channels, Mitochondria, Signal Transduction, Reactive Oxygen Species

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Calcium, ATP, and ROS: a mitochondrial love-hate triangle

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