Evidence map›Paper›PMID 26076475›Full record

ArticlePloS one2015

Anti-Inflammatory and Anti-Thrombotic Effects of the Fungal Metabolite Galiellalactone in Apolipoprotein E-Deficient Mice.

Franziska Bollmann, Sven Jäckel, Lisa Schmidtke, Katharina Schrick, Christoph Reinhardt, Kerstin Jurk, Zhixiong Wu, Ning Xia, Huige Li, Gerhard Erkel and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Franziska BollmannDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Sven JäckelCenter for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Lisa SchmidtkeDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Katharina SchrickDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Christoph ReinhardtCenter for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Kerstin JurkCenter for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Zhixiong WuDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Ning XiaDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Huige LiDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Gerhard ErkelDepartment of Molecular Biotechnology and Systems Biology, Technical University Kaiserslautern, Kaiserslautern, Germany.
Ulrich WalterCenter for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Hartmut KleinertDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Andrea PautzDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEUniversity of Kaiserslautern · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients suffering from chronic inflammatory diseases have an increased mortality risk resulting from cardiovascular disorders due to enhanced atherosclerotic and thrombotic events. Until now, it is not completely understood in which way an abnormal expression of pro-inflammatory mediators contributes to this elevated cardiovascular risk, but there is a need for new drugs that on the one hand suppress the expression of pro-inflammatory mediators and on the other hand inhibit arterial platelet adhesion. Thus, we analyzed the anti-inflammatory and anti-thrombotic capacity of the fungal metabolite Galiellalactone in atherosclerosis-prone apolipoprotein E-deficient mice. Treatment of the mice with Galiellalactone lowered the inflammatory expression profile and improved blood clotting times, as well as platelet adhesion to the injured common carotid artery. The results indicate that administration of Galiellalactone is able to reduce the extent of inflammation and arterial platelet adhesion in this mouse model.

Indexed as

AnimalsAnti-Inflammatory AgentsApolipoproteins EAtherosclerosisBlood CoagulationCarotid ArteriesCarotid Artery ThrombosisCytokinesDisease Models, AnimalFibrinolytic AgentsLactonesMiceMice, Inbred C57BLMice, KnockoutPlatelet AdhesivenessWhole Blood Coagulation TimeAnti-Inflammatory AgentsApolipoproteins ECytokinesFibrinolytic AgentsgaliellalactoneLactones

Identifiers

PMID26076475
PMCPMC4468253
OpenAlexW2199819393

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.