Evidence map›Paper›PMID 27822682›Full record

ReviewCurrent atherosclerosis reports2016

The Different Facets of Dyslipidemia and Hypertension in Atherosclerosis.

Jessica Hurtubise, Krystie McLellan, Kevin Durr, Oluwadara Onasanya, Daniel Nwabuko, Joseph Fomusi Ndisang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 9 pooled it
6.1field-weighted citation impact, top 3% 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

138 citing papers in PubMed, 9 syntheses or guidelines pooled it, 247 citations in OpenAlex.

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  6. The Impact of Chromium Supplementation on Blood Pressure: A Systematic Review and Dose-Response Meta‑Analysis of Randomized‑Controlled Trials.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2021
    Pooled it
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  15. Ameliorative Effects ofFoods (Basel, Switzerland) · 2026
    Article
  16. CD80Cell communication and signaling : CCS · 2026
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78 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

6 authors at 1 institution in 1 country.

Jessica HurtubiseDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Krystie McLellanDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Kevin DurrDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Oluwadara OnasanyaDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Daniel NwabukoDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Joseph Fomusi NdisangDepartment of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada. joseph.ndisang@usask.ca.
University of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors. Correspondingly, the factors are redirected by chemo-attractants and pro-inflammatory cytokines into the intima of the vasculature, where monocytes differentiate into macrophages taking up oxidized LDL uncontrollably to form foam cells and atherosclerotic lesions. Moreover, endothelial damage also causes loss of vasomotor activity, disproportionate vascular contractility, and elevation of blood pressure in dyslipidemic patients, while in hypertensive patients, further elevation of blood pressure occurs, creating a self-perpetuating vicious cycle that aggravates the development and progression of atherosclerotic lesions. This review offers an in-depth analysis of atherosclerosis and the related interplay between dyslipidemia/hypertension and critically appraises the current diagnosis, etiology, and therapeutic options.

Indexed as

AnimalsAtherosclerosisDyslipidemiasHumansHypertensionInflammationLipoproteinsOxidative StressLipoproteinsDyslipidemiaEndothelial dysfunctionHigh-density lipoproteinHypertensionInflammationLow-density lipoproteinOxidative stress

Identifiers

PMID27822682
OpenAlexW2554934526

What Socratic holds

Textmetadata
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 Socratic graph.