Evidence map›Paper›PMID 24701228›Full record

ArticleArchives of medical science : AMS2014

Thrombin inhibition by dabigatran attenuates atherosclerosis in ApoE deficient mice.

Simon Pingel, Vedat Tiyerili, Jens Mueller, Nikos Werner, Georg Nickenig, Cornelius Mueller

Open access · goldAbstract read
In one paragraph

Article in Archives of medical science : AMS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

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  10. Intracerebral hemorrhage and thrombin-induced alterations in cerebral microvessel matrix.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
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  15. Where the Action Is-Leukocyte Recruitment in Atherosclerosis.Frontiers in cardiovascular medicine · 2021
    Review
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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

6 authors at 1 institution in 1 country.

Simon PingelMedizinische Klinik und Poliklinik II, Universitätsklinikum, Bonn, Germany.
Vedat TiyeriliMedizinische Klinik und Poliklinik II, Universitätsklinikum, Bonn, Germany.
Jens MuellerInstitut für experimentelle Hämatologie und Transfusionsmedizin, Universitätsklinikum, Bonn, Germany.
Nikos WernerMedizinische Klinik und Poliklinik II, Universitätsklinikum, Bonn, Germany.
Georg NickenigMedizinische Klinik und Poliklinik II, Universitätsklinikum, Bonn, Germany.
Cornelius MuellerMedizinische Klinik und Poliklinik II, Universitätsklinikum, Bonn, Germany.
University Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAtherosclerosis is a chronic inflammatory disease characterized by endothelial cell damage, infiltration, proliferation and accumulation of macrophages, lymphocytes and transformed vascular smooth muscle cells within the vascular wall and procoagulation processes involving activation of plasmatic coagulation events and platelets. Numerous studies suggested a close interaction between thrombin action and atherogenesis, but possibly underlying mechanisms are multiple and specific treatment options were missing until now. MATERIAL AND

methodsAtherosclerosis prone 12 weeks old ApoE(-/-) mice were fed a cholesterol rich diet for 4 weeks and were concomitantly treated orally with placebo or the thrombin inhibitor dabigatran (1.2 g/kg/day).

resultsThe thrombin time (HEMOCLOT(®)) was significant extended in dabigatran treated animals. Vascular oxidative stress was significantly reduced during thrombin inhibition, as assessed by L012 chemiluminescence in aortic segments (212 ±84 vs. 69 ±21 RLU/s/mg dry weight, p = 0.048). Organ chamber experiments of isolated aortic rings showed that dabigatran treatment significantly improved endothelium-derived vasorelaxation (p < 0.001). Dabigatran treated mice developed less atherosclerotic lesions (6.2 ±0.2% vs. 9 ±1.1%, p = 0.037) and showed less infiltration of atherosclerotic lesions with macrophages (2.59 ±0.3% vs. 5.14 ±0.7%, p = 0.0046), as determined by systematic histological and immunohistological analyses of the aortic root. Blood pressure, body weight and food intake were not altered by the treatment.

conclusionsThe thrombin inhibitor dabigatran reduces vascular oxidative stress and inflammation, improves endothelial function and decreases atherosclerosis in mice.

Indexed as

atherosclerosisdabigatranendothelial functionthrombin inhibition

Identifiers

PMID24701228
PMCPMC3953984
OpenAlexW1602638715

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.