The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.
Nitric Oxide Insufficiency, Platelet Activation, and Arterial Thrombosis
Abstract
Abstract—Nitric oxide (NO) was originally discovered as a vasodilator product of the endothelium. Over the last 15 years, this vascular mediator has been shown to have important antiplatelet actions as well. By activating guanylyl cyclase, inhibiting phosphoinositide 3-kinase, impairing capacitative calcium influx, and inhibiting cyclooxygenase-1, endothelial NO limits platelet activation, adhesion, and aggregation. Platelets are also an important source of NO, and this platelet-derived NO pool limits recruitment of platelets to the platelet-rich thrombus. A deficiency of bioactive NO is associated with arterial thrombosis in animal models, individuals with endothelial dysfunction, and patients with a deficiency of the extracellular antioxidant enzyme glutathione peroxidase-3. This enzyme catalyzes the reduction of hydrogen and lipid peroxides, which limits the availability of these reactive oxygen species to react with and inactivate NO. The complex biochemical reactions that underlie the function and inactivation of NO in the vasculature represent an important set of targets for therapeutic intervention for the prevention and treatment of arterial thrombotic disorders.
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Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“NO has a vasodilating effect and inhibits platelet aggregation [63].”
From Mediterranean Diet as an Antioxidant: The Impact on Metabolic Health and Overall Wellbeing (2021) · cites this paper as [63]
In the citing paper
“NO has a vasodilating effect and inhibits platelet aggregation [63].”
From Mediterranean Diet as an Antioxidant: The Impact on Metabolic Health and Overall Wellbeing (2021) · cites this paper as [63]
In the citing paper
“The activation of platelets is mediated by NO through the soluble guanylate cyclase (sGC) pathway.”
From Recent advances in thromboresistant and antimicrobial polymers for biomedical applications: just say yes to nitric oxide (NO) (2016) · cites this paper as [121]
In the citing paper
“The NO produced by eNOS contributes to the thromboresistant properties of the endothelial lining of blood vessels by inhibiting platelet activation.”
From Recent advances in thromboresistant and antimicrobial polymers for biomedical applications: just say yes to nitric oxide (NO) (2016) · cites this paper as [121]
In the citing paper
“In addition, the cGMP increases cyclic adenosine monophosphate (cAMP) levels indirectly through phosphodiesterase III, which will also decrease the intracellular calcium concentration.”
From Recent advances in thromboresistant and antimicrobial polymers for biomedical applications: just say yes to nitric oxide (NO) (2016) · cites this paper as [121]
In the citing paper
“The NO activated sGC ultimately results in reduced intracellular calcium, inhibition of platelet phosphoinositide 3-kinase (PI3), and reduced affinity as well as number of surface membrane fibrinogen binding sites on platelets (GPIIb/IIIa).117,121–126”
From Recent advances in thromboresistant and antimicrobial polymers for biomedical applications: just say yes to nitric oxide (NO) (2016) · cites this paper as [121]
Citations
Cites
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Biochemistry of nitric oxide and its redox-activated forms
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Self-citationUpregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors
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Nitric oxide circulates in mammalian plasma primarily as an S-nitroso adduct of serum albumin.
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Research works printed but not linked: 18
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- 10.1161/res.81.5.865 · DOI
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- 10.1161/atvb.19.8.2017 · DOI
- Voetsch B, Bierl C, Damasceno BP, Annichino-Bizzacchi JM, Arruda VR, Loscalzo J. A novel promoter polymorphism in the plasma glutathione peroxidase gene associated with arterial ischemic stroke in the young. Circulation. 2000;102:II-704.
- 10.1161/atvb.18.8.1248 · DOI
Cited by
Sorted by citations
Benavente-García, O., & Castillo, J. (2008) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf8006568 · Cited by 1,158
Webb, A. J., Patel, N., Loukogeorgakis, S., Okorie, M., Aboud, Z., Misra, S., Rashid, R., Miall, P., Deanfield, J., Benjamin, N., et al. (2008) · Hypertension · doi:10.1161/hypertensionaha.107.103523 · Cited by 1,078
Krötz, F., Sohn, H., & Pohl, U. (2004) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000145574.90840.7d · Cited by 1,030
Endothelial Function: A Critical Determinant in Atherosclerosis?
Landmesser, U., Hornig, B., & Drexler, H. (2004) · Circulation · doi:10.1161/01.cir.0000129501.88485.1f · Cited by 851
HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3
Nofer, J., van der Giet, M., Tölle, M., Wolinska, I., Lipinski, K. V. W., Baba, H. A., Tietge, U. J. F., Gödecke, A., Ishii, I., Kleuser, B., et al. (2004) · Journal of Clinical Investigation · doi:10.1172/jci18004 · Cited by 705
Metadata
- Authors
- Loscalzo, J.
- Affiliations
- Boston University (US)
- Corresponding author
- Loscalzo, Joseph
- ORCID
- Loscalzo, Joseph
- Venue
- Circulation Research
- Published
- 2001-04-27
- Volume
- 88
- Issue
- 8
- Pages
- 756-762
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2113684546
- Cited by
- 612
- References
- 80
- Citations by year
- 2026: 18 · 2025: 21 · 2024: 22 · 2023: 21 · 2022: 22 · 2021: 19 · 2020: 25 · 2019: 15 · 2018: 28 · 2017: 25 · 2016: 16 · 2015: 24 · 2014: 27 · 2013: 28 · 2012: 29
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL61795, HL 55993, HL58976, R01HL058976, P50HL055993)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Keywords
- nitric oxide, platelet activation, arterial thrombosis, endothelial dysfunction, glutathione peroxidase 3, phosphatidylinositol 3-kinase, cyclooxygenase-1, guanylate cyclase, platelet aggregation, thromboprophylaxis
- MeSH terms
- Animals, Arteries, Blood Platelets, Endothelium, Vascular, Glutathione Peroxidase, Humans, Nitric Oxide, Thrombosis, Vasodilator Agents, Platelet Activation, Reactive Oxygen Species, Nitric Oxide Donors
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