Evidence map›Paper›PMID 19851078›Full record

ReviewJournal of vascular research2010

Complex regulation and function of the inflammatory smooth muscle cell phenotype in atherosclerosis.

Anthony Wayne Orr, Nicole E Hastings, Brett R Blackman, Brian R Wamhoff

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of vascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed, 1 pooled it
6.4field-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

137 citing papers in PubMed, 1 synthesis or guideline pooled it, 280 citations in OpenAlex.

  1. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
    Pooled it
  2. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
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  7. Genetic silencing of KChannels (Austin, Tex.) · 2025
    Article
  8. Molecular Targets for Intracranial Aneurysm Treatment.International journal of molecular sciences · 2025
    Review
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77 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 3 institutions in 1 country.

Anthony Wayne OrrDepartment of Pathology, Louisiana State University Health Sciences Center, Shreveport, La., USA.
Nicole E Hastings
Brett R Blackman
Brian R Wamhoff
University of Virginia · USHemoShear (United States) · USLouisiana State University Health Sciences Center Shreveport · US

Funding

Engineering an Atherosclerosis-Resistant EndotheliumR01HL080956 · NHLBI · UNIVERSITY OF VIRGINIA · PI SCHWARTZ, MARTIN A · 2007 to 2011
$3.6M
Hemodynamic Adaptation of Intercellular Junctions in Human EndotheliumR01HL082836 · NHLBI · UNIVERSITY OF VIRGINIA · PI BLACKMAN, BRETT R · 2007 to 2011
$2.1M
Calcium-dependent Regulation of Smooth Muscle PhenotypeR01HL081682 · NHLBI · UNIVERSITY OF VIRGINIA · PI WAMHOFF, BRIAN ROBERT · 2006 to 2010
$1.5M
NHLBI NIH HHS HL080956NHLBI NIH HHS HL081682NHLBI NIH HHS HL082836NHLBI NIH HHS R01 HL080956NHLBI NIH HHS R01 HL081682NHLBI NIH HHS R01 HL082836
6 · The paper itself

Abstract

Vascular smooth muscle cell (SMC) phenotypic modulation plays a key role in atherosclerosis and is classically defined as a switch from a 'contractile' phenotype to a 'synthetic' phenotype, whereby genes that define the contractile SMC phenotype are suppressed and proliferation and/or migratory mechanisms are induced. There is also evidence that SMCs may take on a 'proinflammatory' phenotype, whereby SMCs secrete cytokines and express cell adhesion molecules, e.g. IL-8, IL-6, and VCAM-1, respectively, which may functionally regulate monocyte and macrophage adhesion and other processes during atherosclerosis. Factors that drive the inflammatory phenotype are not limited to cytokines but also include hemodynamic forces imposed on the blood vessel wall and intimate interaction of endothelial cells with SMCs, as well as changes in matrix composition in the vessel wall. However, it is critical to recognize that our understanding of the complex interaction of these multiple signal inputs has only recently begun to shed light on mechanisms that regulate the inflammatory SMC phenotype, primarily through models that attempt to recreate this environment ex vivo. The goal of this review is to summarize our current knowledge in this area and identify some of the key unresolved challenges and questions requiring further study.

Indexed as

AnimalsAtherosclerosisCell Adhesion MoleculesCell ProliferationExtracellular Matrix ProteinsGene Expression RegulationHemodynamicsHumansInflammationInflammation MediatorsMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeProtein Processing, Post-TranslationalSignal TransductionStress, MechanicalCell Adhesion MoleculesExtracellular Matrix ProteinsInflammation Mediators

Identifiers

PMID19851078
PMCPMC2842170
OpenAlexW2090372317

What OpenQuestion 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 OpenQuestion graph.