Signaling by S-nitrosylation in the heart
Open accessAbstract
Nitric oxide is a gaseous signaling molecule that is well-known for the Nobel prize-winning research that defined nitric oxide as a physiological regulator of blood pressure in the cardiovascular system. Nitric oxide can signal via the classical pathway involving activation of guanylyl cyclase or by a post-translational modification, referred to as S-nitrosylation (SNO) that can occur on cysteine residues of proteins. As proteins with cysteine residues are common, this allows for amplification of the nitric oxide signaling. This review will focus on the possible mechanisms through which SNO can alter protein function in cardiac cells, and the role of SNO occupancy in these mechanisms. The specific mechanisms that regulate protein SNO, including redox-dependent processes, will also be discussed. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".
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Some studies have described that endothelial overexpression of NOX2 increases endothelial dysfunction.
“Some studies have described that endothelial overexpression of NOX2 increases endothelial dysfunction (88, 676).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [676]
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Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation
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- Authors
- Murphy, E., Kohr, M., Menazza, S., Nguyen, T., Evangelista, A., Sun, J., & Steenbergen, C.
- Affiliations
- National Institutes of Health (US)
- Johns Hopkins University (US)
- Corresponding author
- Murphy, Elizabeth
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2014-08
- Volume
- 73
- Pages
- 18-25
- ISSN
- 0022-2828 (ISSN-L)
- PMC
- PMC4214076
- OpenAlex
- W2091174988
- Cited by
- 82
- References
- 74
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 6 · 2020: 4 · 2019: 9 · 2018: 9 · 2017: 12 · 2016: 9 · 2015: 11 · 2014: 8
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (K99HL114721, R00HL114721, R01HL039752, ZIAHL006059, ZIAHL002066)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Keywords
- S-nitrosylation, nitric oxide signaling, heart, cysteine residues, post-translational modification, redox signaling, guanylate cyclase, cardiomyocytes, protein function regulation
- MeSH terms
- Animals, Heart, Humans, Nitric Oxide, Oxidation-Reduction, Protein Processing, Post-Translational, Signal Transduction, S-Nitrosothiols
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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