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The Role of Mitochondria in Reactive Oxygen Species Metabolism and Signaling
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Oxidative stress is considered a major contributor to the etiology of both “normal” senescence and severe pathologies with serious public health implications. Several cellular sources, including mitochondria, are known to produce significant amounts of reactive oxygen species (ROS) that may contribute to intracellular oxidative stress. Mitochondria possess at least 10 known sites that are capable of generating ROS, but they also feature a sophisticated multilayered ROS defense system that is much less studied. This review summarizes the current knowledge about major components involved in mitochondrial ROS metabolism and factors that regulate ROS generation and removal at the level of mitochondria. An integrative systemic approach is applied to analysis of mitochondrial ROS metabolism, which is “dissected” into ROS generation, ROS emission, and ROS scavenging. The in vitro ROS‐producing capacity of several mitochondrial sites is compared in the metabolic context and the role of mitochondria in ROS‐dependent intracellular signaling is discussed.
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“The succinate concentration in different tissues and mitochondria is in the submillimolar range under aerobic conditions [22,72,73], indicating that complex II is not working at maximal velocity under 'standard conditions'.”
From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [22]
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“The highly effective mitochondrial antioxidative defense system encompasses the thioredoxin/peroxiredoxin system as well as the glutathione/glutathione peroxidase system (overview in [22,117]).”
From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [22]
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Metadata
- Authors
- Starkov, A. A.
- Affiliations
- Cornell University (US)
- Corresponding author
- Starkov, Anatoly A.
- ORCID
- Starkov, Anatoly A.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2008-12
- Volume
- 1147
- Issue
- 1
- Pages
- 37-52
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC2869479
- OpenAlex
- W2053022803
- Cited by
- 846
- References
- 86
- Citations by year
- 2026: 39 · 2025: 39 · 2024: 42 · 2023: 66 · 2022: 67 · 2021: 78 · 2020: 74 · 2019: 55 · 2018: 42 · 2017: 46 · 2016: 50 · 2015: 39 · 2014: 38 · 2013: 41 · 2012: 39
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG014930, P01AG014930)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondria, reactive oxygen species, oxidative stress, ROS signaling, reactive oxygen species scavenging, aging, cellular senescence
- MeSH terms
- Humans, Mitochondria, Signal Transduction, Reactive Oxygen Species, Oxidative Stress
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