ReviewImmunologic research2002
Oxidases and oxygenases in regulation of vascular nitric oxide signaling and inflammatory responses.
Review in Immunologic research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 31 citations in OpenAlex.
- The Etiology and Molecular Mechanism Underlying Smooth Muscle Phenotype Switching in Intimal Hyperplasia of Vein Graft and the Regulatory Role of microRNAs.Frontiers in cardiovascular medicine · 2022Review
- Vascular TSP1-CD47 signaling promotes sickle cell-associated arterial vasculopathy and pulmonary hypertension in mice.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- 3-nitrotyrosine modified proteins in atherosclerosis.Disease markers · 2015Review
- Mitochondrial reactive oxygen species mediate GPCR-induced TACE/ADAM17-dependent transforming growth factor-alpha shedding.Molecular biology of the cell · 2009Article
- Nitric oxide promotes distant organ protection: evidence for an endocrine role of nitric oxide.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Sickle cell disease and nitric oxide: a paradigm shift?The international journal of biochemistry & cell biology · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (.NO) is a freely diffusible inter- and intracellular messenger produced by a variety of mammalian cells including vascular endothelium, neurons, smooth muscle cells, macrophages, neutrophils, platelets, and pulmonary epithelium. In smooth muscle cells, platelets, and neutrophils, .NO raises intracellular cyclic guanasine 5'-monophosphate levels by reacting with the catalytic heme domain of guanylate cylase, to activate it, thus leading to vasorelaxation, inhibition of platelet aggregation and inhibition of platelet and inflammatory cell adhesion to endothelium. The physiologic actions of .NO are highly dependent on changes in steady-state concentrations of reactive species and tissue-oxidant defense mechanisms. Vessel wall oxidases and oxygenases, in particular, are critical sources of oxygen radical production and can lead to an overall impairment of vascular .NO signaling, via the metalloprotein and free radical-mediated consumption of this vasoactive molecule. Vascular oxidase and oxygenase activities can thus account for the functional inactivation of .NO, leading to a prooxidative milieu and chronic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.