Evidence map›Paper›PMID 21439758›Full record

ReviewJournal of vascular surgery2011

Vascular biology of metabolic syndrome.

Daynene Vykoukal, Mark G Davies

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of vascular surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 3 pooled it
9.6field-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

55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 124 citations in OpenAlex.

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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.

Daynene VykoukalVascular Biology and Therapeutics Program, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, TX77030, USA.
Mark G Davies
Houston Methodist · US

Funding

"Phospholipids, Metabolic Syndrome and Response to Injury"R01HL086968 · NHLBI · UNIVERSITY OF ROCHESTER · PI DAVIES, MARK GLYNN · 2007 to 2011
$1.9M
uPA RECEPTOR SIGNALING AND CELL MIGRATIONK08HL067746 · NHLBI · UNIVERSITY OF ROCHESTER · PI DAVIES, MARK GLYNN · 2001 to 2005
$616k
NHLBI NIH HHS HL086968NHLBI NIH HHS K08 HL067746NHLBI NIH HHS R01 HL086968
6 · The paper itself

Abstract

The metabolic syndrome is a constellation of clinical risk factors comprising atherogenic dyslipidemia (low high-density lipoprotein and high triglycerides levels), elevated blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state accompanied by an increased risk for cardiovascular disease and type 2 diabetes mellitus. The adipose tissue of obese humans contains increased numbers of macrophages, and once activated, these macrophages are responsible for the expression of most of the tissue's tumor necrosis factor (TNF)-α and interleukin (IL)-6. Chronic inflammation associated with visceral obesity induces altered lipoprotein metabolism and insulin resistance in the liver. Adipocytes secrete a variety of hormones, cytokines, growth factors, and other bioactive substances, conceptualized as adipocytokines, including plasminogen activator inhibitor 1 (PAI-1), TNF-α, leptin, and adiponectin. The dysregulation of these adipokines contributes to the pathogenesis of obesity. Adipose tissue-resident macrophages and adipocytes in the adipose tissue combined with the consequences of hyperglycemia, altered lipoproteins, and hyperinsulinemia in the vasculature and within organ microcirculation lead to dysfunctional endothelia and a proinflammatory state. Metabolic syndrome thus represents a combination of synergistic vascular pathologies that lead to an accelerated atherogenic state that compromises the ability of the patient to satisfactorily respond to humoral, cellular, and mechanical stresses.

Indexed as

Signal TransductionAdipokinesAdipose TissueAnimalsBlood CoagulationDyslipidemiasEndothelium, VascularHumansHyperglycemiaHypertensionInflammationInflammation MediatorsInsulin ResistanceMetabolic SyndromeObesityAdipokinesInflammation Mediators

Identifiers

PMID21439758
PMCPMC3136643
OpenAlexW2143957228

What OpenQuestion holds

Textmetadata
LicenceTDM
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.