Evidence map›Paper›PMID 24968272›Full record

ReviewInternational journal of molecular sciences2014

Endothelial dysfunction in chronic inflammatory diseases.

Curtis M Steyers, Francis J Miller

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 8 pooled it
15.2field-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

233 citing papers in PubMed, 8 syntheses or guidelines pooled it, 456 citations in OpenAlex.

  1. Effects of Walnut (Juglans regia L.) on Blood Pressure and Endothelial Function in Adults: A Systematic Review and Dose-Response Meta-Analysis.Journal of human nutrition and dietetics : the official journal of the British Dietetic Association · 2026
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173 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.

Curtis M SteyersDepartment of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA. curtis-m-steyers@uiowa.edu.
Francis J MillerDepartment of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA. francis-miller@uiowa.edu.
University of Iowa · US

Funding

Regulation of the Nox1 NADPH Oxidase in Vascular Smooth Muscle CellsI01BX001729 · VA · IOWA CITY VA MEDICAL CENTER · PI MILLER, FRANCIS J · 2012 to 2020
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BLRD VA I01 BX001729
6 · The paper itself

Abstract

Chronic inflammatory diseases are associated with accelerated atherosclerosis and increased risk of cardiovascular diseases (CVD). As the pathogenesis of atherosclerosis is increasingly recognized as an inflammatory process, similarities between atherosclerosis and systemic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel diseases, lupus, psoriasis, spondyloarthritis and others have become a topic of interest. Endothelial dysfunction represents a key step in the initiation and maintenance of atherosclerosis and may serve as a marker for future risk of cardiovascular events. Patients with chronic inflammatory diseases manifest endothelial dysfunction, often early in the course of the disease. Therefore, mechanisms linking systemic inflammatory diseases and atherosclerosis may be best understood at the level of the endothelium. Multiple factors, including circulating inflammatory cytokines, TNF-α (tumor necrosis factor-α), reactive oxygen species, oxidized LDL (low density lipoprotein), autoantibodies and traditional risk factors directly and indirectly activate endothelial cells, leading to impaired vascular relaxation, increased leukocyte adhesion, increased endothelial permeability and generation of a pro-thrombotic state. Pharmacologic agents directed against TNF-α-mediated inflammation may decrease the risk of endothelial dysfunction and cardiovascular disease in these patients. Understanding the precise mechanisms driving endothelial dysfunction in patients with systemic inflammatory diseases may help elucidate the pathogenesis of atherosclerosis in the general population.

Indexed as

AnimalsArthritisAtherosclerosisCholesterol, LDLEndothelium, VascularHumansInflammationInflammatory Bowel DiseasesTumor Necrosis Factor-alphaCholesterol, LDLTumor Necrosis Factor-alpha

Identifiers

PMID24968272
PMCPMC4139785
OpenAlexW2110926368

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.