Evidence map›Paper›PMID 23316317›Full record

ArticleJournal of the American Heart Association2012

Growth differentiation factor-15 deficiency inhibits atherosclerosis progression by regulating interleukin-6-dependent inflammatory response to vascular injury.

Gabriel A Bonaterra, Stefanie Zügel, Joel Thogersen, Sabrina A Walter, Uwe Haberkorn, Jens Strelau, Ralf Kinscherf

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 7% 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

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The Effect of Thyroid Function on GDF15 Levels.International journal of molecular sciences · 2025
    Article
  16. GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Review

31 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

7 authors at 3 institutions in 1 country.

Gabriel A BonaterraInstitute of Anatomy and Cell Biology, Department of Medical Cell Biology, University of Marburg, Marburg, Germany.
Stefanie Zügel
Joel Thogersen
Sabrina A Walter
Uwe Haberkorn
Jens Strelau
Ralf Kinscherf
Philipps University of Marburg · DEHeidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowth differentiation factor (GDF)-15 is a distant and divergent member of the transforming growth factor-β superfamily (TGF-β) . There is growing evidence indicating the involvement of GDF-15 in various pathologies. Expression of GDF-15 is induced under conditions of inflammation and increased GDF-15 serum levels are suggested as a risk factor for cardiovascular diseases. METHODS AND

resultsWe show here that GDF-15 and proinflammatory cytokine interleukin (IL)-6 levels are highly increased (5-fold) in cultured oxidized low-density lipoproteins-stimulated peritoneal macrophages derived from GDF-15(+/+)/apolipoprotein (apo) E(-/-), mice. Notably, IL-6 induction on oxidized low-density lipoproteins stimulation is completely abolished in the absence of GDF-15. Consistent with our in vitro data GDF-15 mRNA expression and protein levels are upregulated (2.5- to 6-fold) in the atherosclerotic vessel wall of GDF-15(+/+)/apoE(-/-) mice after a cholesterol-enriched diet. GDF-15 deficiency inhibits lumen stenosis (52%) and (18)FDG uptake (34%) in the aortic arch despite increased serum triglyceride/cholesterol levels and elevated body weight. Immunohistomorphometric investigations of atherosclerotic lesions reveal a decreased percentage of inflammatory CD11b(+) (57%) or IL-6(+), leukocytes, and apoptotic cells (74%) after 20 weeks. However, the total number of macrophages and cell density in atherosclerotic lesions of the innominate artery are increased in GDF-15(-/-)/apoE(-/-) mice.

conclusionsOur data suggest that GDF-15 is involved in orchestrating atherosclerotic lesion progression by regulating apoptotic cell death and IL-6-dependent inflammatory responses to vascular injury.

Indexed as

Disease ProgressionAnimalsAorta, ThoracicAtherosclerosisBody WeightBrachiocephalic TrunkCholesterolGrowth Differentiation Factor 15InflammationInterleukin-6MiceMice, KnockoutPositron-Emission TomographyReal-Time Polymerase Chain ReactionRNA, MessengerTriglyceridesCholesterolGrowth Differentiation Factor 15Interleukin-6RNA, MessengerTriglyceridesatherosclerosisGDF‐15inflammationinterleukins

Identifiers

PMID23316317
PMCPMC3540664
OpenAlexW2140348286

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.