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Cited by 347Mitochondrial Function and PathologyRedox biology and oxidative stressNitric Oxide and Endothelin Effects

The DOI matches its Crossref record; 181 of the 181 references it cites were found in a registry or an index.

Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

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Daiber, Andreas·2010·Biochimica et Biophysica Acta (BBA) - Bioenergetics
DOI 10.1016/j.bbabio.2010.01.032
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Abstract

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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Research works printed but not linked: 2

  1. Feelisch, 1993, Biotransformation to nitric oxide of organic nitrates in comparison to other nitrovasodilators, Eur. Heart J., 14, 123
  2. Wenzel, 2007, Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus, Atherosclerosis

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Metadata

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)
DOI
10.1016/j.bbabio.2010.01.032
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
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 (medical) › 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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