Signal Transduction by Mitochondrial Oxidants
Open accessAbstract
The production of mitochondrial reactive oxygen species occurs as a consequence of aerobic metabolism. Mitochondrial oxidants are increasingly viewed less as byproducts of metabolism and more as important signaling molecules. Here, I review several notable examples, including the cellular response to hypoxia, aspects of innate immunity, the regulation of autophagy, and stem cell self-renewal capacity, where evidence suggests an important regulatory role for mitochondrial oxidants.
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In healthy situations, the generation of ROS by eNOS, mitochondria, or XO is limited.
“In healthy situations, the generation of ROS by eNOS, mitochondria, or XO is limited, and in the case of mitochondria, it is probably more related to signaling pathways (289, 290).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [290]
In healthy situations, mitochondrial ROS generation is probably more related to signaling pathways.
“In healthy situations, the generation of ROS by eNOS, mitochondria, or XO is limited, and in the case of mitochondria, it is probably more related to signaling pathways (289, 290).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [290]
Low physiological concentrations of mitochondrial oxidants mediate essential cellular signaling pathways.
“Importantly, although mitochondrial ROS can propagate cellular damage, low physiological concentrations of mitochondrial oxidants have been shown to mediate a number of essential cellular signaling pathways (290).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [290]
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References 55 · Cited by 390
- Authors
- Finkel, T.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Finkel, Toren
- ORCID
- Finkel, Toren
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 287
- Issue
- 7
- Pages
- 4434-4440
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3281633
- OpenAlex
- W2065527667
- Cited by
- 390
- References
- 55
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 20 · 2023: 25 · 2022: 28 · 2021: 43 · 2020: 29 · 2019: 29 · 2018: 27 · 2017: 24 · 2016: 29 · 2015: 35 · 2014: 31 · 2013: 27 · 2012: 19
- FWCI
- 2.26
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ellison Medical Foundation
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial reactive oxygen species, redox signaling, hypoxia response, innate immunity, autophagy regulation, stem cell self-renewal, aerobic metabolism
- MeSH terms
- Animals, Hypoxia, Humans, Immunity, Innate, Mitochondria, Stem Cells, Signal Transduction, Oxidants
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