The DOI matches its Crossref record; 106 of the 106 references it cites were found in a registry or an index.
Nitric Oxide and Mitochondrial Signaling: From Physiology to Pathophysiology
Abstract
Nitric oxide (NO) has been known for many years to bind to cytochrome C oxidase, the terminal acceptor in the mitochondrial electron transport chain, in competition with oxygen. This interaction may be significant in vivo and explain some of the biological actions of NO. In this article we review the evidence showing that binding of NO to cytochrome C oxidase elicits intracellular signaling events, including the diversion of oxygen to nonrespiratory substrates and the generation of reactive oxygen species. We discuss findings indicating that these NO-elicited events act as triggers by which mitochondria modulate signal transduction cascades involved in the induction of cellular defense mechanisms and adaptive responses. We also discuss instances in which the effects of NO on the electron transport chain might lead to mitochondrial dysfunction and pathology.
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“In the last 15 years it has been established that the mitochondrion is a physiological target for NO (ref. 8).”
From Nitrate and nitrite in biology, nutrition and therapeutics (2009) · cites this paper as [8]
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In the citing paper
“In a doubleblind, placebo-controlled, cross over study, Larsen et al. found that the oxygen cost during standardized exercise was reduced after 3 days of dietary supplementation with sodium nitrate compared with placebo.124”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [124]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“There was no difference in lactate formation, indicating that there was no compensatory increase in glycolytic energy contribution, and thus metabolic efficiency seemed to be improved.”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [124]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Recent data suggest that many of the biologic effects of nitrite involve interaction with mitochondria.124,125”
From Nitrate-Nitrite-Nitric Oxide Pathway: Implications for Anesthesiology and Intensive Care (2010) · cites this paper as [124]
Experimental — accuracy not yet measuredIn the citing paper
“The high affinity and rapid binding to ferrous heme are important biologically for the activation of sGC to generate the second messenger cGMP and the regulation of mitochondrial respiration at CcOx (9–16).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [12]
In the citing paper
“The high affinity and rapid binding to ferrous heme are important biologically for the activation of sGC to generate the second messenger cGMP and the regulation of mitochondrial respiration at CcOx (9–16).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [12]
In the citing paper
“Other studies indicate that stabilization of HIF-1α by NO leads to an increase in glycolytic pathways [217] as well as activation of AMPK [218].”
From Signaling and stress: The redox landscape in NOS2 biology (2015) · cites this paper as [218]
In the citing paper
“A principal regulator of the response to hypoxia is the hypoxia-inducible factor (HIF) family of transcription factors (31, 61, 115, 165, 177, 185, 221, 282–286, 316, 327).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [115]
In the citing paper
“Moreover, superoxide is known to react very rapidly with NO (107), generating a damaging peroxynitrite (ONOO−) radical (98, 144, 246), which can impair proteins involved in electron transport (261).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [98]
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Metadata
- Authors
- Erusalimsky, J. D., & Moncada, S.
- Affiliations
- University College London (GB)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2007-12
- Volume
- 27
- Issue
- 12
- Pages
- 2524-2531
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2048626265
- Cited by
- 336
- References
- 105
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 15 · 2023: 6 · 2022: 11 · 2021: 15 · 2020: 9 · 2019: 10 · 2018: 6 · 2017: 16 · 2016: 13 · 2015: 19 · 2014: 34 · 2013: 30 · 2012: 21
- FWCI
- 3.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- 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
- Keywords
- nitric oxide, cytochrome c oxidase, mitochondrial signaling, electron transport chain, reactive oxygen species, signal transduction, cellular defense mechanisms, mitochondrial dysfunction
- MeSH terms
- Animals, Calcium, Electron Transport Complex IV, Endothelium, Vascular, Glycolysis, Homeostasis, Humans, Mitochondria, Multienzyme Complexes, Nitric Oxide, Oxygen, Transcription Factors, Signal Transduction, Cell Hypoxia, Apoptosis, Protein Serine-Threonine Kinases, Reactive Oxygen Species, Cytoprotection, Endothelial Cells, Membrane Potential, Mitochondrial, AMP-Activated Protein Kinases
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