Evidence map›Paper›PMID 23966666›Full record

ArticleJournal of lipid research2013

Statins stimulate the production of a soluble form of the receptor for advanced glycation end products.

Patricia Quade-Lyssy, Anna Maria Kanarek, Markus Baiersdörfer, Rolf Postina, Elzbieta Kojro

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Current Status of Primary, Secondary, and Tertiary Prevention of Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. AGE-RAGE Axis in the Pathophysiology of Chronic Lower Limb Ischemia and a Novel Strategy for Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2020
    Review
  19. Review
  20. AGE-RAGE Stress in the Pathophysiology of Pulmonary Hypertension and its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2019
    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

5 authors at 1 institution in 1 country.

Patricia Quade-LyssyInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University, D-55128 Mainz, Germany.
Anna Maria Kanarek
Markus Baiersdörfer
Rolf Postina
Elzbieta Kojro
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The beneficial effects of statin therapy in the reduction of cardiovascular pathogenesis, atherosclerosis, and diabetic complications are well known. The receptor for advanced glycation end products (RAGE) plays an important role in the progression of these diseases. In contrast, soluble forms of RAGE act as decoys for RAGE ligands and may prevent the development of RAGE-mediated disorders. Soluble forms of RAGE are either produced by alternative splicing [endogenous secretory RAGE (esRAGE)] or by proteolytic shedding mediated by metalloproteinases [shed RAGE (sRAGE)]. Therefore we analyzed whether statins influence the production of soluble RAGE. Lovastatin treatment of either mouse alveolar epithelial cells endogenously expressing RAGE or HEK cells overexpressing RAGE caused induction of RAGE shedding, but did not influence secretion of esRAGE from HEK cells overexpressing esRAGE. Lovastatin-induced secretion of sRAGE was also evident after restoration of the isoprenylation pathway, demonstrating a correlation of sterol biosynthesis and activation of RAGE shedding. Lovastatin-stimulated induction of RAGE shedding was completely abolished by a metalloproteinase ADAM10 inhibitor. We also demonstrate that statins stimulate RAGE shedding at low physiologically relevant concentrations. Our results show that statins, due to their cholesterol-lowering effects, increase the soluble RAGE level by inducing RAGE shedding, and by doing this, might prevent the development of RAGE-mediated pathogenesis.

Indexed as

Animalsbeta-CyclodextrinsBridged Bicyclo Compounds, HeterocyclicCell LineCholesterolDose-Response Relationship, DrugFarnesyl-Diphosphate FarnesyltransferaseHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLovastatinMiceReceptor for Advanced Glycation End ProductsReceptors, ImmunologicSolubilityTricarboxylic Acidsbeta-CyclodextrinsBridged Bicyclo Compounds, HeterocyclicCholesterolFarnesyl-Diphosphate FarnesyltransferaseHydroxymethylglutaryl-CoA Reductase InhibitorsLovastatinmethyl-beta-cyclodextrinReceptor for Advanced Glycation End ProductsReceptors, Immunologicsqualestatin 1Tricarboxylic AcidsADAM 10atherosclerosisdiabetic complicationshypercholesterolemia

Identifiers

PMID23966666
PMCPMC3793609
OpenAlexW2020351781

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.