Evidence map›Paper›PMID 22614668›Full record

ReviewCardiovascular journal of Africa2012

Endothelial dysfunction: the early predictor of atherosclerosis.

Mashudu Mudau, Amanda Genis, Amanda Lochner, Hans Strijdom

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular journal of Africa, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 3 pooled it
11.1field-weighted citation impact, top 1% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

242 citing papers in PubMed, 3 syntheses or guidelines pooled it, 506 citations in OpenAlex.

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182 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Mashudu MudauDepartment of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa.
Amanda Genis
Amanda Lochner
Hans Strijdom
Stellenbosch University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the discovery in the 1980s that nitric oxide (NO) is in fact the elusive endothelium-derived relaxing factor, it has become evident that NO is not only a major cardiovascular signalling molecule, but that changes in its bioavailability are crucial in determining whether atherosclerosis will develop or not. Sustained high levels of harmful circulating stimuli associated with cardiovascular risk factors such as diabetes mellitus elicit responses in endothelial cells that appear sequentially, namely endothelial cell activation and endothelial dysfunction (ED). ED, characterised by reduced NO bioavailability, is now recognised by many as an early, reversible precursor of atherosclerosis. The pathogenesis of ED is multifactorial; however, oxidative stress appears to be the common underlying cellular mechanism in the ensuing loss of vaso-active, inflammatory, haemostatic and redox homeostasis in the body's vascular system. The role of ED as a pathophysiological link between early endothelial cell changes associated with cardiovascular risk factors and the development of ischaemic heart disease is of importance to basic scientists and clinicians alike.

Indexed as

AtherosclerosisOxidative StressEndothelium, VascularHumansNitric OxideRisk FactorsNitric Oxide

Identifiers

PMID22614668
PMCPMC3721957
OpenAlexW2124860950

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.