Cross talk between mitochondria and NADPH oxidases
Open accessAbstract
Reactive oxygen species (ROS) play an important role in physiological and pathological processes. In recent years, a feed-forward regulation of the ROS sources has been reported. The interactions between the main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. This work summarizes the latest findings on the role of cross talk between mitochondria and NADPH oxidases in pathophysiological processes. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain conditions may stimulate NADPH oxidases. This cross talk between mitochondria and NADPH oxidases, therefore, may represent a feed-forward vicious cycle of ROS production, which can be pharmacologically targeted under conditions of oxidative stress. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension, and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions.
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Recent work indicates that normalizing a disease state by direct inhibition of a single source of oxidative stress can be a feasible approach.
“Recent work indicates that this can be a feasible approach (206, 207, 234, 836).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [234]
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Redox activation of Nrf2 & NF-κB: A double end sword?
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Which NADPH Oxidase Isoform Is Relevant for Ischemic Stroke? The Case for Nox 2
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Anti-Aging Potentials of Methylene Blue for Human Skin Longevity
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Cardiovascular disease and the biology of aging
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- Authors
- Dikalov, S.
- Affiliations
- Emory University (US)
- Corresponding author
- Dikalov, Sergey
- ORCID
- Dikalov, Sergey
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 51
- Issue
- 7
- Pages
- 1289-1301
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3163726
- OpenAlex
- W2011124873
- Cited by
- 783
- References
- 186
- Citations by year
- 2026: 26 · 2025: 31 · 2024: 35 · 2023: 51 · 2022: 54 · 2021: 59 · 2020: 69 · 2019: 53 · 2018: 62 · 2017: 70 · 2016: 50 · 2015: 63 · 2014: 59 · 2013: 60 · 2012: 39
- FWCI
- 4.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL094469, HL094469)
- 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 › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- mitochondria, NADPH oxidase, reactive oxygen species, mitochondrial ROS production, feedforward control, oxidative stress, mitochondria-targeted antioxidants, redox state, mitochondrial dysfunction, aging, atherosclerosis, diabetes mellitus, hypertension, degenerative neurological disorders
- MeSH terms
- Aging, Angiotensin II, Animals, Antioxidants, Diabetes Mellitus, Humans, Hypertension, Mitochondria, Organophosphorus Compounds, Oxidation-Reduction, Piperidines, Rabbits, Superoxide Dismutase, Xanthine Oxidase, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Neurodegenerative Diseases, Atherosclerosis, Mice, Rats, Nitric Oxide Synthase Type III
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