Electrophilic nitro-fatty acids: anti-inflammatory mediators in the vascular compartment
Open accessAbstract
Vascular inflammatory disorders are often associated with both decreased NO bioavailability and a lack of responsiveness to NO, a consequence of impaired NO biosynthesis, dysregulated l-arginine metabolism, endothelial nitric oxide synthase (eNOS) uncoupling and NO consumption induced by redox reactions of NO. The latter is mediated via oxidative inflammatory conditions altering NO-dependent endothelial function, including vascular tone and cell proliferation. The redox reactions of NO and byproducts such as nitrite can react to yield electrophilic nitro-fatty acid derivatives (NO(2)-FAs) and exemplify a biochemical convergence of reactions participating in NO and lipid signaling. NO(2)-FAs represent a novel therapeutic strategy to treat vascular disorders by improving endothelial dysfunction through enhancing NO signaling and blocking vascular smooth muscle proliferation, inflammation, and maladaptive remodeling.
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Nitration of both fatty acids and guanine nucleotides has been shown to elicit responses that are protective against inflammatory tissue injury.
“nitration of both fatty acids and guanine nucleotides has been shown to elicit responses that are protective against inflammatory tissue injury[115, 116].”
From Current perspectives and challenges in understanding the role of nitrite as an integral player in nitric oxide biology and therapy (2011) · cites this paper as [116]
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- Authors
- Khoo, N. K., & Freeman, B. A.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Khoo, Nicholas KH
- ORCID
- Khoo, Nicholas KH
- Venue
- Current Opinion in Pharmacology
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 10
- Issue
- 2
- Pages
- 179-184
- ISSN
- 1471-4892 (ISSN-L)
- PMC
- PMC2843800
- OpenAlex
- W1984981225
- Cited by
- 56
- References
- 51
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 4 · 2016: 2 · 2015: 7 · 2014: 3 · 2013: 11 · 2012: 7
- FWCI
- 5.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL 64937, R01HL064937, R37HL058115, HL8115)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- nitric oxide, nitric oxide bioavailability, endothelial dysfunction, vascular inflammation, endothelial nitric oxide synthase uncoupling, arginine metabolism, nitrite, redox reactions, lipid signaling, vascular smooth muscle cell proliferation, vascular remodeling, anti-inflammatory mediators
- MeSH terms
- Animals, Cardiovascular Diseases, Endothelium, Vascular, Fatty Acids, Humans, Inflammation, Models, Biological, Nitric Oxide, Nitro Compounds, Peroxisome Proliferator-Activated Receptors, Cell Proliferation, NF-E2-Related Factor 2, Heme Oxygenase-1, Nitric Oxide Synthase Type III
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