Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species
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This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial damage suppressed angiotensin-II-dependent increase in Nox1 and oxidative stress. In another example hypoxia was used as a stimulator of mitochondrial ROS formation and by using pharmacological and genetic inhibitors, a role of mitochondrial ROS for the induction of NADPH oxidase via PKCvarepsilon was demonstrated. The third model was based on cell death by serum withdrawal that promotes the production of ROS in human 293T cells by stimulating both the mitochondria and Nox1. By superior molecular biological methods the authors showed that mitochondria were responsible for the fast onset of ROS formation followed by a slower but long-lasting oxidative stress condition based on the activation of an NADPH oxidase (Nox1) in response to the fast mitochondrial ROS formation. Finally, a cross-talk between mitochondria and NADPH oxidases (Nox2) was shown in nitroglycerin-induced tolerance involving the mitochondrial permeability transition pore and ATP-sensitive potassium channels. The use of these redox signaling pathways as pharmacological targets is briefly discussed.
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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 [206]
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Self-citationEnzyme Inhibition by Peroxynitrite-Mediated Tyrosine Nitration and Thiol Oxidation
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Reactive Oxygen Species in Inflammation and Tissue Injury
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- Authors
- Daiber, A.
- Affiliations
- University Medical Center of the Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Daiber, Andreas
- ORCID
- Daiber, Andreas
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 1797
- Issue
- 6-7
- Pages
- 897-906
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W2029195231
- Cited by
- 347
- References
- 181
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 14 · 2023: 15 · 2022: 22 · 2021: 26 · 2020: 27 · 2019: 17 · 2018: 19 · 2017: 28 · 2016: 28 · 2015: 22 · 2014: 27 · 2013: 34 · 2012: 25
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Johannes Gutenberg-Universität Mainz
- Actavis Deutschland
- 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
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- redox signaling, mitochondria, NADPH oxidase, reactive oxygen species, mitochondrial permeability transition pore, ATP-sensitive potassium channels, angiotensin II, hypoxia, protein kinase C epsilon, serum deprivation, cell death, mitochondrial reactive oxygen species, oxidative stress, nitroglycerin tolerance, NOX1, NOX2, mitochondrial membrane potential
- MeSH terms
- Mitochondrial Permeability Transition Pore, Aging, Angiotensin II, Animals, Humans, Hypertension, Mitochondria, Models, Biological, Oxidation-Reduction, Potassium Channels, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Feedback, Physiological, Reactive Nitrogen Species, Myocytes, Smooth Muscle, Mitochondrial Membrane Transport Proteins, In Vitro Techniques
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