Cited by 490Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressCardiovascular Health and Disease Prevention

S -Nitrosylation in Cardiovascular Signaling

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Lima, Brian, Forrester, Michael T., Hess, Douglas T., Stamler, Jonathan S.·2010·Circulation Research

Abstract

Abstract : Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be the gaseous molecule nitric oxide (NO). Although soluble guanylyl cyclase (which generates cyclic guanosine monophosphate, cGMP) was the first identified receptor for NO, it has become increasingly clear that NO exerts a ubiquitous influence in a cGMP-independent manner. In particular, many, if not most, effects of NO are mediated by S -nitrosylation, the covalent modification of a protein cysteine thiol by an NO group to generate an S -nitrosothiol (SNO). Moreover, within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G protein–coupled receptor–mediated, or shear-induced endothelium-derived NO bioactivity) is understood to involve a central role for SNOs, acting both as second messengers and signal effectors. Furthermore, essential roles for S -nitrosylation have been implicated in virtually all major functions of NO in the cardiovascular system. Here, we review the basic biochemistry of S -nitrosylation (and denitrosylation), discuss the role of S -nitrosylation in the vascular and cardiac functions of NO, and identify current and potential clinical applications.

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Crossref · 10.1161/circresaha.109.207381

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  • Global kinetic analysis suggests that the main source of NO2· in vivo may be the decomposition of peroxynitrite.

    “Global kinetic analysis of the reactions involved suggests that the main source of NO2· in vivo may be the decomposition of peroxynitrite (585).”
  • NO regulates the activities of enzymes and signaling proteins by S-nitrosylation of thiol moieties.

    “Furthermore, NO regulates the activities of enzymes and signaling proteins by S-nitrosylation of thiol moieties (2).”

    From Dietary nitrate, nitric oxide, and restenosis (2011) · cites this paper as [2]

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Authors
Lima, B., Forrester, M. T., Hess, D. T., & Stamler, J. S.
Affiliations
Duke University (US)
Corresponding author
Stamler, Jonathan S.
Venue
Circulation Research
Published
2010-03-05
Volume
106
Issue
4
Pages
633-646
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2143004446
Cited by
490
References
175
Citations by year
2026: 11 · 2025: 14 · 2024: 16 · 2023: 16 · 2022: 22 · 2021: 28 · 2020: 24 · 2019: 22 · 2018: 31 · 2017: 27 · 2016: 35 · 2015: 39 · 2014: 44 · 2013: 39 · 2012: 48
FWCI
5.17
Type
journal article
Language
en
Open access
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (HL-075443)
  • National Heart, Lung, and Blood Institute (R01HL095463, R01HL091876, R01HL059130, P01HL075443, R01HL096673)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords
S-nitrosylation, nitric oxide, S-nitrosothiols, denitrosylation, cGMP-independent signaling, G protein-coupled receptors, cardiovascular signaling, vascular function, cardiac function, second messengers, clinical application
MeSH terms
Animals, Cardiovascular Diseases, Cardiovascular System, Endothelium, Vascular, Cyclic GMP, Humans, Inflammation, Myocardium, Nitric Oxide, Protein Processing, Post-Translational, Vascular Resistance, Signal Transduction, Apoptosis, Neovascularization, Physiologic, S-Nitrosothiols, Endothelium-Dependent Relaxing Factors

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