Evidence map›Paper›PMID 28982031›Full record

ArticleThrombosis research2017

Direct thrombin inhibition with dabigatran attenuates pressure overload-induced cardiac fibrosis and dysfunction in mice.

Anping Dong, Paul Mueller, Fanmuyi Yang, Liping Yang, Andrew Morris, Susan S Smyth

Open access · greenAbstract read
In one paragraph

Article in Thrombosis research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  11. Protease Nexin-1 in the Cardiovascular System: Wherefore Art Thou?Frontiers in cardiovascular medicine · 2021
    Review
  12. Article
  13. Therapeutic molecular targets of SSc-ILD.Journal of scleroderma and related disorders · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Shared and distinct mechanisms of fibrosis.Nature reviews. Rheumatology · 2019
    Review
  18. Article
  19. Direct oral anticoagulants and vitamin K antagonists are linked to differential profiles of cardiac function and lipid metabolism.Clinical research in cardiology : official journal of the German Cardiac Society · 2019
    Observational
  20. Review
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.

Anping DongDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States; Lexington VA Medical Center, 1101 Veterans Drive, Lexington, KY 40502, United States.
Paul MuellerDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States. Electronic address: muellerp@ohsu.edu.
Fanmuyi YangDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States. Electronic address: Fanmuyi.Yang@cchmc.org.
Liping YangDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States. Electronic address: lpyang2@email.uky.edu.
Andrew MorrisDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States; Lexington VA Medical Center, 1101 Veterans Drive, Lexington, KY 40502, United States. Electronic address: amorr6@email.uky.edu.
Susan S SmythDivision of Cardiovascular Medicine, The Gill Heart Institute, 741 S. Limestone Street, 252 BBSRB, Lexington, KY 40536-0509, United States; Lexington VA Medical Center, 1101 Veterans Drive, Lexington, KY 40502, United States. Electronic address: Susan.Smyth@uky.edu.
Lexington VA Health Care System · US

Funding

Kentucky Center for Clinical and Translational ScienceUL1TR001998 · NCATS · UNIVERSITY OF KENTUCKY · PI HARTMANN, KATHERINE E, KERN, PHILIP A · 2016 to 2025
$34.2M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI REN, HONGMEI · 2012 to 2017
$13.7M
THROMBOSPONDIN1 MEDIATES MACROPHAGE INFILTRATION INTO ADIPOSE TISSUE AND PROMOTEP20RR021954 · NCRR · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2008 to 2011
$8.3M
NRSA Training CoreTL1TR001997 · NCATS · UNIVERSITY OF KENTUCKY · PI PENDERGAST, JULIE S, STOOPS, WILLIAM WALTON · 2016 to 2025
$4.2M
Lysolipid Signaling in Cardovascular DiseaseR01HL078663 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SMYTH, SUSAN S. · 2004 to 2013
$2.5M
Interdisciplinary Cardiovascular Training ProgramT32HL072743 · NHLBI · UNIVERSITY OF KENTUCKY · PI RANDALL, DAVID C · 2004 to 2013
$1.3M
NCATS NIH HHS TL1 TR001997NCATS NIH HHS UL1 TR001998NCRR NIH HHS P20 RR021954NHLBI NIH HHS R01 HL078663NHLBI NIH HHS T32 HL072743NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

introductionThe multifunctional serine protease thrombin exerts proinflammatory and profibrotic cellular effects that may contribute to cardiac remodeling. This study was designed to investigate whether direct thrombin inhibition with dabigatran attenuates myocardial injury in the setting of pressure overload-induced heart failure. MATERIAL AND

methodsTransverse aortic constriction (TAC) surgery was performed on C57Bl/6J male mice to elicit cardiac hypertrophy. TAC, or sham, mice were randomly assigned to receive chow supplemented with the oral anticoagulant, dabigatran etexilate, or placebo.

resultsDabigatran did not affect cardiac hypertrophy, as measured by heart weight-to-body weight or the heart weight-to-tibia length, although a non-significant reduction in myocardial hypertrophic markers (ANP, BNP and MHC) occurred. Dabigatran reduced perivascular fibrosis by 25%, interstitial fibrosis by 54%, and the expression of myocardial fibrosis markers collagen I & III, MMP9, SMA, and PAR-1. These changes were associated with significant improvement in both coronary flow reserve and global left ventricular function. In cultured cardiac fibroblasts, dabigatran decreased thrombin and PAR-1-mediated collagen deposition by 30% and 37%, respectively.

conclusionsDabigatran attenuates cardiac fibrosis in the setting of pressure overload and improves coronary flow reserve and global cardiac function possibly by inhibiting thrombin activity and down-regulating PAR-1 expression in the absence of an effect on cardiomyocyte hypertrophy.

Indexed as

AnimalsDabigatranDisease Models, AnimalFibrosisHumansMaleMiceMyocardiumThrombinDabigatranThrombinCardiac fibrosisDirect thrombin inhibitorProtease-activated receptorThrombin

Identifiers

PMID28982031
PMCPMC5722681
OpenAlexW2757981801

What OpenQuestion holds

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Registered trials

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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.