Evidence map›Paper›PMID 18489853›Full record

ReviewCurrent atherosclerosis reports2008

Inflammatory signaling through leukotriene receptors in atherosclerosis.

Magnus Bäck

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Activation of group VI phospholipase A2 isoforms in cardiac endothelial cells.American journal of physiology. Cell physiology · 2011
    Article
  12. Article
  13. Leukotriene signaling in atherosclerosis and ischemia.Cardiovascular drugs and therapy · 2009
    Review
  14. Review
  15. Activation by C5a of endothelial cell caspase 8 and cFLIP.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009
    Article
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

1 author at 1 institution in 1 country.

Magnus BäckDepartment of Cardiology and Center for Molecular Medicine, Karolinska University Hospital, 17176 Stockholm, Sweden. Magnus.Back@ki.se
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The atherosclerotic lesion is a site of local production of the lipid-derived inflammatory mediators known as leukotrienes. This production leads to autocrine and paracrine activation of leukotriene receptors of the BLT and CysLT receptor subtypes expressed on leukocytes and structural cells within the vascular wall. Studies in mice, rats, and rabbits have revealed a key role for leukotriene signaling in atherosclerosis, abdominal aneurysms, and intimal hyperplasia. In addition, a major atherosclerotic immune activation may be leukotriene-dependent through mediation of leukocyte cross-talk within the atherosclerotic lesion. Furthermore, leukotrienes induce endothelium-dependent and independent vascular responses. Finally, recent findings indicate that leukotriene-dependent degradation of the extracellular matrix may link this pathway to atherosclerotic plaque instability. Taken together, the leukotriene pathway may represent a putative therapeutic target in the treatment of atherosclerotic vessel disease.

Indexed as

AnimalsAtherosclerosisBlood VesselsChemotaxis, LeukocyteDisease Models, AnimalHumansInflammationInflammation MediatorsLeukocytesLeukotrienesMatrix MetalloproteinasesReceptors, LeukotrieneInflammation MediatorsLeukotrienesMatrix MetalloproteinasesReceptors, Leukotriene

Identifiers

PMID18489853
OpenAlexW1983565010

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.