ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Differential regulation of metabolism by nitric oxide and S-nitrosothiols in endothelial cells.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- β-Cell-selective regulation of gene expression by nitric oxide.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Endothelial cell and T-cell crosstalk: Targeting metabolism as a therapeutic approach in chronic inflammation.British journal of pharmacology · 2021Review
- Inhibition of oxidative metabolism by nitric oxide restricts EMCV replication selectively in pancreatic beta-cells.The Journal of biological chemistry · 2020Article
- Nitric Oxide in Macrophage Immunometabolism: Hiding in Plain Sight.Metabolites · 2020Review
- 'SNO'-Storms Compromise Protein Activity and Mitochondrial Metabolism in Neurodegenerative Disorders.Trends in endocrinology and metabolism: TEM · 2017Review
- Nitric Oxide Synthase-2-Derived Nitric Oxide Drives Multiple Pathways of Breast Cancer Progression.Antioxidants & redox signaling · 2017Review
- Similarities in the Metabolic Reprogramming of Immune System and Endothelium.Frontiers in immunology · 2017Review
- Maternal high-fat diet impairs cardiac function in offspring of diabetic pregnancy through metabolic stress and mitochondrial dysfunction.American journal of physiology. Heart and circulatory physiology · 2016Article
- Effect of Dietary Bioactive Compounds on Mitochondrial and Metabolic Flexibility.Diseases (Basel, Switzerland) · 2016Review
- Alpha-lipoic acid supplementation protects enzymes from damage by nitrosative and oxidative stress.Biochimica et biophysica acta · 2016Article
- Signaling and stress: The redox landscape in NOS2 biology.Free radical biology & medicine · 2015Review
- Respiratory substrates regulate S-nitrosylation of mitochondrial proteins through a thiol-dependent pathway.Chemical research in toxicology · 2014Article
- S-Nitrosation of monocarboxylate transporter 1: inhibition of pyruvate-fueled respiration and proliferation of breast cancer cells.Free radical biology & medicine · 2014Article
- Inhibition of autophagy and glycolysis by nitric oxide during hypoxia-reoxygenation impairs cellular bioenergetics and promotes cell death in primary neurons.Free radical biology & medicine · 2013Article
- Effect of nitric oxide on naphthoquinone toxicity in endothelial cells: role of bioenergetic dysfunction and poly (ADP-ribose) polymerase activation.Biochemistry · 2013Article
- Nitrosative stress and redox-cycling agents synergize to cause mitochondrial dysfunction and cell death in endothelial cells.Redox biology · 2013Article
- Cytochrome c-mediated formation of S-nitrosothiol in cells.The Biochemical journal · 2012Article
- Is There a Link between Mitochondrial Reserve Respiratory Capacity and Aging?Journal of aging research · 2012Article
- Assessing bioenergetic function in response to oxidative stress by metabolic profiling.Free radical biology & medicine · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
S-nitrosation of thiols in key proteins in cell signaling pathways is thought to be an important contributor to nitric oxide (NO)-dependent control of vascular (patho)physiology. Multiple metabolic enzymes are targets of both NO and S-nitrosation, including those involved in glycolysis and oxidative phosphorylation. Thus it is important to understand how these metabolic pathways are integrated by NO-dependent mechanisms. Here, we compared the effects of NO and S-nitrosation on both glycolysis and oxidative phosphorylation in bovine aortic endothelial cells using extracellular flux technology to determine common and unique points of regulation. The compound S-nitroso-L-cysteine (L-CysNO) was used to initiate intracellular S-nitrosation since it is transported into cells and results in stable S-nitrosation in vitro. Its effects were compared with the NO donor DetaNONOate (DetaNO). DetaNO treatment caused only a decrease in the reserve respiratory capacity; however, L-CysNO impaired both this parameter and basal respiration in a concentration-dependent manner. In addition, DetaNO stimulated extracellular acidification rate (ECAR), a surrogate marker of glycolysis, whereas L-CysNO stimulated ECAR at low concentrations and inhibited it at higher concentrations. Moreover, a temporal relationship between NO- and S-nitrosation-mediated effects on metabolism was identified, whereby NO caused a rapid impairment in mitochondrial function, which was eventually overwhelmed by S-nitrosation-dependent processes. Taken together, these results suggest that severe pharmacological nitrosative stress may differentially regulate metabolic pathways through both intracellular S-nitrosation and NO-dependent mechanisms. Moreover, these data provide insight into the role of NO and related compounds in vascular (patho)physiology.
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Registered trials
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