Evidence map›Paper›PMID 18487233›Full record

ReviewCardiovascular research2008

Cytokines and atherosclerosis: a comprehensive review of studies in mice.

Robert Kleemann, Susanne Zadelaar, Teake Kooistra

Abstract readReview
In one paragraph

Review in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
263citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

263 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Plasma chemokines indicate enhanced bleeding in patients with chronic coronary syndrome undergoing percutaneous coronary stenting.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
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  11. Neutrophil Extracellular Traps in Atherosclerosis: Research Progress.International journal of molecular sciences · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Sonodynamic therapy for the treatment of atherosclerosis.Journal of pharmaceutical analysis · 2024
    Review
  18. Article
  19. Review
  20. Review

203 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.

Robert KleemannTNO-BioSciences, Gaubius-Laboratory, Department of Vascular and Metabolic Diseases, PO Box 2215, 2301 CE Leiden, The Netherlands. robert.kleemann@tno.nl
Susanne Zadelaar
Teake Kooistra

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the past few years, inflammation has emerged as a major driving force of atherosclerotic lesion development. It is now well-established that from early lesion to vulnerable plaque formation, numerous cellular and molecular inflammatory components participate in the disease process. The most prominent cells that invade in evolving lesions are monocyte-derived macrophages and T-lymphocytes. Both cell types produce a wide array of soluble inflammatory mediators (cytokines, chemokines) which are critically important in the initiation and perpetuation of the disease. This review summarizes the currently available information from mouse studies on the contribution of a specified group of cytokines expressed in atherosclerotic lesions, viz. interleukins (IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, IL-20) and macrophage-associated cytokines [tumour necrosis factor-alpha (TNF-alpha); macrophage migration inhibitory factor (MIF); interferon-gamma (IFN-gamma); colony stimulating factors G-CSF,-M-CSF,-GM-CSF) to atherogenesis. Emphasis is put on the consistency of the effects of these cytokines, i.e. inasmuch an effect depends on the experimental approach applied (overexpression/deletion, strain, gender, dietary conditions, and disease stage). An important outcome of this survey is (i) that only for a few cytokines there is sufficient consistent data allowing classifying them as typically proatherogenic (IL-1, IL-12, IL-18, MIF, IFN-gamma, TNF-alpha, and M-CSF) or antiatherogenic (IL-10) and (ii) that some cytokines (IL-4, IL-6 and GM-CSF) can exert pro- or anti-atherogenic effects depending on the experimental conditions. This knowledge can be used for improved early detection, prevention and treatment of atherosclerosis.

Indexed as

Signal TransductionAnimalsAtherosclerosisColony-Stimulating FactorsCytokinesDisease Models, AnimalInflammationInterferon-gammaInterleukinsMacrophage Migration-Inhibitory FactorsMiceTumor Necrosis Factor-alphaColony-Stimulating FactorsCytokinesInterferon-gammaInterleukinsMacrophage Migration-Inhibitory FactorsTumor Necrosis Factor-alpha

Identifiers

PMID18487233
PMCPMC2492729

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.