Evidence map›Paper›PMID 18276911›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2008

Role of smooth muscle cells in the initiation and early progression of atherosclerosis.

Amanda C Doran, Nahum Meller, Coleen A McNamara

Open access · greenAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 362 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
362citing papers in PubMed, 3 pooled it
16.1field-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

362 citing papers in PubMed, 3 syntheses or guidelines pooled it, 799 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020
    Pooled it
  4. Article
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  12. Pathogenic mechanisms in Fabry disease.Frontiers in medicine · 2026
    Review
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  17. Article
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  19. Article
  20. The role of tribbles homolog 2 in cell proliferation.Cell communication and signaling : CCS · 2025
    Review

302 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

3 authors at 1 institution in 1 country.

Amanda C DoranCardiovascular Division/Department of Medicine, the Cardiovascular Research Center, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.
Nahum Meller
Coleen A McNamara
University of Virginia · US

Funding

ROLE OF LIPOXYGENASES IN ATHEROGENESIS IN DIABETES MELLITUSP01HL055798 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HEDRICK, CATHERINE C · 1995 to 2016
$28.4M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Local B-1 Regulation of AtherosclerosisR01HL136098 · NHLBI · UNIVERSITY OF VIRGINIA · PI MCNAMARA, COLEEN A · 2017 to 2020
$3.1M
ID3 REGULATION OF SMOOTH MUSCLE CELL PROLIFERATIONR01HL062522 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MCNAMARA, COLEEN A · 1999 to 2008
$2.1M
NHLBI NIH HHS P01 HL055798NHLBI NIH HHS P01 HL-55798NHLBI NIH HHS R01 HL062522NHLBI NIH HHS R01 HL136098NHLBI NIH HHS R01 HL-62522
6 · The paper itself

Abstract

The initiation of atherosclerosis results from complex interactions of circulating factors and various cell types in the vessel wall, including endothelial cells, lymphocytes, monocytes, and smooth muscle cells (SMCs). Recent reviews highlight the role of activated endothelium and inflammatory cell recruitment in the initiation of and progression of early atherosclerosis. Yet, human autopsy studies, in vitro mechanistic studies, and in vivo correlative data suggest an important role for SMCs in the initiation of atherosclerosis. SMCs are the major producers of extracellular matrix within the vessel wall and in response to atherogenic stimuli can modify the type of matrix proteins produced. In turn, the type of matrix present can affect the lipid content of the developing plaque and the proliferative index of the cells that are adherent to it. SMCs are also capable of functions typically attributed to other cell types. Like macrophages, SMCs can express a variety of receptors for lipid uptake and can form foam-like cells, thereby participating in the early accumulation of plaque lipid. Like endothelial cells, SMCs can also express a variety of adhesion molecules such as vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 to which monocytes and lymphocytes can adhere and migrate into the vessel wall. In addition, through these adhesion molecules, SMCs can also stabilize these cells against apoptosis, thus contributing to the early cellularity of the lesion. Like many cells within the developing plaque, SMCs also produce many cytokines such as PDGF, transforming growth factor-beta, IFNgamma, and MCP-1, all of which contribute to the initiation and propagation of the inflammatory response to lipid. Recent advances in SMC-specific gene modulation have enhanced our ability to determine the role of SMCs in early atherogenesis.

Indexed as

AtherosclerosisCytokinesDisease ProgressionExtracellular MatrixHumansLipid MetabolismMacrophagesMonocytesMuscle, Smooth, VascularCytokines

Identifiers

PMID18276911
PMCPMC2734458
OpenAlexW2146917818

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.