The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Oxidative stress caused by mitochondrial calcium overload
Abstract
Mitochondrial oxidative stress has been reported as the result of respiratory complex anomalies, genetic defects, or insufficient oxygen or glucose supply. Although Ca 2+ has no direct effect on respiratory chain function or oxidation/reduction process, mitochondrial Ca 2+ overload can lead to reactive oxygen species (ROS) increase. Even though Ca 2+ is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca 2+ overload is detrimental to mitochondrial function and may present as an important cause of mitochondrial ROS generation. Possible mechanisms include Ca 2+ stimulated increase of metabolic rate, Ca 2+ stimulated nitric oxide production, Ca 2+ induced cytochrome c dissociation, Ca 2+ induced cardiolipin peroxidation, Ca 2+ induced mitochondrial permeability transition pore opening with release of cytochrome c and GSH‐antioxidative enzymes, and Ca 2+‐calmodulin dependent protein kinases activation. Different mechanisms may exist under different mitochondrial preparations (isolated mitochondria vs. mitochondria in intact cells), tissue sources, animal species, or inhibitors used. Furthermore, mitochondrial ROS rise can modulate Ca 2+ dynamics and augment Ca 2+ surge. The reciprocal interactions between Ca 2+ induced ROS increase and ROS modulated Ca 2+ upsurge may cause a feedforward, self‐amplified loop createing cellular damage far beyond direct Ca 2+ induced damage.
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Cites
Calcium, ATP, and ROS: a mitochondrial love-hate triangle
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The mitochondrial permeability transition pore and its role in cell death
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Reactive species mechanisms of cellular hypoxia-reoxygenation injury
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Crosstalk signaling between mitochondrial Ca2+ and ROS
Feissner, R. (2009) · Frontiers in Bioscience · doi:10.2741/3303 · Cited by 439
Mitochondrial calcium and oxidative stress as mediators of ischemic brain injury
Starkov, A. A., Chinopoulos, C., & Fiskum, G. (2004) · Cell Calcium · doi:10.1016/j.ceca.2004.02.012 · Cited by 339
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Mitochondrial Dysfunction and Glutamate Excitotoxicity Studied in Primary Neuronal Cultures
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Self-citationCross-talk between calcium and reactive oxygen species signaling
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Cited by
Calcium and ROS: A mutual interplay
Görlach, A., Bertram, K., Hudecova, S., & Krizanova, O. (2015) · Redox Biology · doi:10.1016/j.redox.2015.08.010 · Cited by 1,546
Mitochondrial dysfunction in cell senescence and aging
Miwa, S., Kashyap, S., Chini, E., & von Zglinicki, T. (2022) · Journal of Clinical Investigation · doi:10.1172/jci158447 · Cited by 1,061
Melatonin—A pleiotropic, orchestrating regulator molecule
Hardeland, R., Cardinali, D. P., Srinivasan, V., Spence, D. W., Brown, G. M., & Pandi-Perumal, S. R. (2011) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2010.12.004 · Cited by 843
Initiation and perpetuation of NLRP 3 inflammasome activation and assembly
Elliott, E. I., & Sutterwala, F. S. (2015) · Immunological Reviews · doi:10.1111/imr.12286 · Cited by 821
Oxidative Stress in Cancer Cell Metabolism
Arfin, S., Jha, N. K., Jha, S. K., Kesari, K. K., Ruokolainen, J., Roychoudhury, S., Rathi, B., & Kumar, D. (2021) · Antioxidants · doi:10.3390/antiox10050642 · Cited by 665
Metadata
- Authors
- Peng, T., & Jou, M.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2010-07
- Volume
- 1201
- Issue
- 1
- Pages
- 183-188
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2102738791
- Cited by
- 566
- References
- 32
- FWCI
- 10.16
- Type
- journal article
- Language
- en
- Open access
- closed
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