Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide
Open accessAbstract
The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the anti-inflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H2S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H2S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, besides to its well-known ability to relax vascular smooth muscle cells (VSMCs), and thereby reducing blood pressure. Finally, H2S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H2S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H2S-releasing drugs or using gene therapy to increase endogenous H2S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H2S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications.
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H2S has been implicated as a regulator of both nitric oxide and eicosanoid synthesis.
“H2S has been implicated as a regulator of both nitric oxide and eicosanoid ynthesis [28], [34], [60].”
From Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis (2014) · cites this paper as [60]
Section 6.5 (page unavailable) reports H₂S-induced NO release, supporting its implication in NO regulation. Section 1.0 lists eicosanoids alongside H₂S as endothelial products, but does not say H₂S regulates their synthesis; searches for eicosanoid synthesis and related compounds found no such passage. (LLM, conf=0.85)
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Flagged first, then by citations
Research works printed but not linked: 2
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Cited by
Sorted by citations
Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis
Zayachkivska, O., Havryluk, O., Hrycevych, N., Bula, N., Grushka, O., & Wallace, J. L. (2014) · PLoS ONE · doi:10.1371/journal.pone.0110688 · Cited by 34 · see citing works
“H2S has been implicated as a regulator of both nitric oxide and eicosanoid ynthesis [28,34,60].”
Background
- Authors
- Altaany, Z., Moccia, F., Munaron, L., Mancardi, D., & Wang, R.
- Affiliations
- Lakehead University (CA)
- Bentham Science Publishers (United Arab Emirates) (AE)
- University of Turin (IT)
- Venue
- Current Medicinal Chemistry
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2014-07-06
- Volume
- 21
- Issue
- 32
- Pages
- 3646-3661
- ISSN
- 0929-8673 (ISSN-L)
- OpenAlex
- W2122874855
- Cited by
- 86
- References
- 191
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 12 · 2019: 8 · 2018: 10 · 2017: 9 · 2016: 4 · 2015: 10 · 2014: 4
- FWCI
- 3.99
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Current Medicinal Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Archivio Istituzionale della Ricerca - Università degli Studi del Molise (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
- Keywords
- hydrogen sulfide, endothelial dysfunction, nitric oxide, gasotransmitters, cardiovascular disease, atherosclerosis, angiogenesis, vascular smooth muscle cells, platelet aggregation, gene therapy, endothelial homeostasis
- MeSH terms
- Animals, Endothelium, Vascular, Hydrogen Sulfide, Nitric Oxide, Signal Transduction, Mice, Knockout, Hyperhomocysteinemia, Mice, Nitric Oxide Synthase Type III
About these checks
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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