Evidence map›Paper›PMID 16595793›Full record

ReviewClinical medicine & research2006

Recent advances in understanding endothelial dysfunction in atherosclerosis.

Zhihong Yang, Xiu-Fen Ming

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Clinical medicine & research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT02352740 nacompletednot on this mapstarted 2013, after this paper: background citation

Characterization of the Metabolic Fate of an Oral L-arginine Form in Healthy Subjects Featuring Risk Factors Related to the Metabolic Syndrome.

TypeinterventionalSponsorInstitut National de Recherche pour l'Agriculture, l'Alimentation et l'EnvironnementRan2013Enrolled32ConditionsOverweight, Hypertriglyceridemic WaistArmsA form Arginine, B form Arginine
NCT02354794 nacompletednot on this mapstarted 2014, after this paper: background citation

Effect of Oral Supplementation With One Form of L-arginine on Vascular Endothelial Function in Healthy Subjects Featuring Risk Factors Related to the Metabolic Syndrome.

TypeinterventionalSponsorInstitut National de Recherche pour l'Agriculture, l'Alimentation et l'EnvironnementRan2014 to 2014Enrolled36ConditionsOverweight, Hypertriglyceridemic WaistArmsOne form of arginine, placebo
3 · Its place in the literature

Who cites it

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

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  16. Circadian rhythm and atherosclerosis (Review).Experimental and therapeutic medicine · 2020
    Review
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15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Zhihong YangVascular Biology Laboratory, Department of Medicine, Division of Physiology, University of Fribourg, Rue du Musée 5, CH-1700 Fribourg, Switzerland. zhihong.yang@unifr.ch
Xiu-Fen Ming
University of Fribourg · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the last two decades, it has become evident that decreased bioavailability of endothelial nitric oxide (NO) produced from endothelial NO synthase (eNOS), referred to as endothelial dysfunction, plays a crucial role in the development and progression of atherosclerosis. Much progress has been made in understanding the mechanisms of decreased endothelial NO bioavailability at the levels of regulation of eNOS gene expression, eNOS enzymatic activity and NO inactivation. Initial studies suggest that increasing eNOS gene expression would improve endothelial NO release in the hope of inhibiting the progression of atherosclerosis. Recent experimental studies, however, do not always support this therapeutic concept and show some evidence that overexpression of eNOS in atherosclerosis may be even harmful for the disease progression.Thus, recent research to improve endothelial function in atherosclerosis has focused on regulation of eNOS enzymatic activity and prevention of NO inactivation by oxidative stress. Since the role of oxidative stress in endothelial NO bioavailability has been reviewed in a large number of comprehensive articles, this article focuses on the relevant regulatory mechanisms of eNOS enzymatic activity that are emerging to play a role in endothelial dysfunction in atherosclerosis.

Indexed as

AnimalsCoronary Artery DiseaseDisease ProgressionEndothelium, VascularGene Expression Regulation, EnzymologicHumansNitric OxideNitric Oxide Synthase Type IIIOxidative StressPhosphorylationPolymorphism, GeneticPredictive Value of TestsNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID16595793
PMCPMC1435659
OpenAlexW2161739223

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.