Evidence map›Paper›PMID 27208212›Full record

ReviewThe Biochemical journal2016

The arterial microenvironment: the where and why of atherosclerosis.

Arif Yurdagul, Alexandra C Finney, Matthew D Woolard, A Wayne Orr

Open access · greenAbstract readReview
In one paragraph

Review in The Biochemical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

  1. Hereditary connective tissue disorders in unselected patients with spontaneous cervical artery dissection: a targeted next generation sequencing approach and systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Pooled it
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  13. Polymeric Nanomaterials for Atherosclerosis Diagnosis and Treatment.Polymer science & technology (Washington, D.C.) · 2025
    Review
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  19. Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis.International journal of molecular sciences · 2024
    Article
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41 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

4 authors at 1 institution in 1 country.

Arif YurdagulDepartment of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71130, U.S.A.
Alexandra C FinneyDepartment of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71130, U.S.A.
Matthew D WoolardDepartment of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, U.S.A.
A Wayne OrrDepartment of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, LA 71130, U.S.A. Department of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, U.S.A. aorr@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Leigh Lamonica · 2012 to 2026
$69.1M
Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
NHLBI NIH HHS R01 HL098435NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

The formation of atherosclerotic plaques in the large and medium sized arteries is classically driven by systemic factors, such as elevated cholesterol and blood pressure. However, work over the past several decades has established that atherosclerotic plaque development involves a complex coordination of both systemic and local cues that ultimately determine where plaques form and how plaques progress. Although current therapeutics for atherosclerotic cardiovascular disease primarily target the systemic risk factors, a large array of studies suggest that the local microenvironment, including arterial mechanics, matrix remodelling and lipid deposition, plays a vital role in regulating the local susceptibility to plaque development through the regulation of vascular cell function. Additionally, these microenvironmental stimuli are capable of tuning other aspects of the microenvironment through collective adaptation. In this review, we will discuss the components of the arterial microenvironment, how these components cross-talk to shape the local microenvironment, and the effect of microenvironmental stimuli on vascular cell function during atherosclerotic plaque formation.

Indexed as

AnimalsAtherosclerosisEndothelium, VascularHumansModels, BiologicalPlaque, AtheroscleroticRisk Factorsatherosclerosisextracellular matrixinflammationmicroenvironmentshear stress

Identifiers

PMID27208212
PMCPMC5410666
OpenAlexW2355649199

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.