Evidence map›Paper›PMID 19302038›Full record

ReviewAnnual review of immunology2009

Immune and inflammatory mechanisms of atherosclerosis (*).

Elena Galkina, Klaus Ley

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Annual review of immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01337947 (The Impact of Fitness on Vascular Dysfunction in Adolescents With Type 1 Diabetes), which is not on this map. Cited by 674 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
674citing papers in PubMed, 4 pooled it
33.2field-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.

NCT01337947 completednot on this mapstarted 2011, after this paper: background citation

The Impact of Fitness on Vascular Dysfunction in Adolescents With Type 1 Diabetes

TypeobservationalSponsorUniversity of VirginiaRan2011 to 2013Enrolled32ConditionsType 1 DiabetesArmsDefinity microbubbles
3 · Its place in the literature

Who cites it

674 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,423 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. A Comprehensive Survey of the Relationship betweenArchives of Iranian medicine · 2022
    Pooled it
  5. Trial
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Biomarkers of Cardiovascular Stress: A Historical Review.Journal of cardiovascular development and disease · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Observational
  19. Article
  20. Article

614 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

2 authors at 2 institutions in 1 country.

Elena GalkinaDepartment of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia 23507-1696, USA. galkinev@evms.edu
Klaus Ley
Eastern Virginia Medical School · USLa Jolla Institute for Immunology · US

Funding

ROLE OF LIPOXYGENASES IN ATHEROGENESIS IN DIABETES MELLITUSP01HL055798 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HEDRICK, CATHERINE C · 1995 to 2016
$28.4M
MONOCYTE ADHESION TO ATHEROMA IN GENE TARGETED MICER01HL058108 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LEY, KLAUS F. · 1997 to 2009
$2.6M
NHLBI NIH HHS HL 55798NHLBI NIH HHS HL 58108NHLBI NIH HHS P01 HL055798NHLBI NIH HHS R01 HL058108
6 · The paper itself

Abstract

Atherosclerosis is an inflammatory disease of the wall of large- and medium-sized arteries that is precipitated by elevated levels of low-density lipoprotein (LDL) cholesterol in the blood. Although dendritic cells (DCs) and lymphocytes are found in the adventitia of normal arteries, their number is greatly expanded and their distribution changed in human and mouse atherosclerotic arteries. Macrophages, DCs, foam cells, lymphocytes, and other inflammatory cells are found in the intimal atherosclerotic lesions. Beneath these lesions, adventitial leukocytes organize in clusters that resemble tertiary lymphoid tissues. Experimental interventions can reduce the number of available blood monocytes, from which macrophages and most DCs and foam cells are derived, and reduce atherosclerotic lesion burden without altering blood lipids. Under proatherogenic conditions, nitric oxide production from endothelial cells is reduced and the burden of reactive oxygen species (ROS) and advanced glycation end products (AGE) is increased. Incapacitating ROS-generating NADPH oxidase or the receptor for AGE (RAGE) has beneficial effects. Targeting inflammatory adhesion molecules also reduces atherosclerosis. Conversely, removing or blocking IL-10 or TGF-beta accelerates atherosclerosis. Regulatory T cells and B1 cells secreting natural antibodies are atheroprotective. This review summarizes our current understanding of inflammatory and immune mechanisms in atherosclerosis.

Indexed as

AnimalsArteriesAtherosclerosisCell Adhesion MoleculesCholesterol, LDLCytokinesDendritic CellsGlycation End Products, AdvancedHumansInflammationInflammation MediatorsLeukocytesMacrophagesMast CellsNitric OxideCell Adhesion MoleculesCholesterol, LDLCytokinesGlycation End Products, AdvancedInflammation MediatorsNitric Oxide

Identifiers

PMID19302038
PMCPMC2734407
OpenAlexW2096626379

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.