Evidence map›Paper›PMID 30867376›Full record

ArticleJournal of atherosclerosis and thrombosis2019

Rivaroxaban Suppresses the Progression of Ischemic Cardiomyopathy in a Murine Model of Diet-Induced Myocardial Infarction.

Jingyi Liu, Makoto Nishida, Hiroyasu Inui, Jiuyang Chang, Yinghong Zhu, Kotaro Kanno, Hibiki Matsuda, Masami Sairyo, Takeshi Okada, Hajime Nakaoka and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

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  5. SR-B1-/-ApoE-R61h/h Mice Mimic Human Coronary Heart Disease.Cardiovascular drugs and therapy · 2024
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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

15 authors at 3 institutions in 2 countries.

Jingyi LiuDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Makoto NishidaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Hiroyasu InuiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Jiuyang ChangDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Yinghong ZhuDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Kotaro KannoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Hibiki MatsudaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Masami SairyoDepartment of Cardiology, Kawanishi City Hospital.
Takeshi OkadaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Hajime NakaokaDepartment of Cardiology, Kakogawa Central City Hospital.
Tohru OhamaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Daisaku MasudaRinku General Medical Center.
Masahiro KosekiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Shizuya YamashitaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine.
Osaka University · JPKagawa Prefectural Central Hospital · JPOsaka Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimA direct oral anti-coagulant, FXa inhibitor, has been applied to the clinical treatment of myocardial infarction (MI). Experimental studies in mice indicated that FXa inhibitors reduced atherosclerosis and prevented cardiac dysfunction after coronary ligation. These studies suggested that protease-activated receptor (PAR) 2, a major receptor of activated FX, may play an important role in atherosclerosis and cardiac remodeling.

methodsThe effects of a FXa inhibitor, rivaroxaban, were investigated in a new murine model of ischemic cardiomyopathy (ICM) using SR-BI KO/ApoeR61

resultsHypo E mice were fed rivaroxaban-containing (n=49) or control chow diets (n=126) after the induction of MI. The survival curve of the rivaroxaban-treated group 2 weeks after the induction of MI was improved significantly as compared with the non-treatment group (survival rate: 75.5% vs. 47.4%, respectively, p=0.0012). Echocardiography and the expression of BNP showed that rivaroxaban attenuated heart failure. Histological analyses revealed that rivaroxaban reduced aortic atherosclerosis and coronary occlusion, and markedly attenuated cardiac fibrosis. Rivaroxaban treatment decreased cardiac PAR2 levels and pro-inflammatory genes. In vitro, rivaroxaban application demonstrated the increase of cell viability against hypoxia in cardiac myocytes and the reduction of hypoxia-induced inflammation and fibrosis-related molecules in cardiac fibroblasts. The effects of the PAR2 antagonist against hypoxia-induced inflammation were comparable to rivaroxaban in cardiac fibroblasts.

conclusionsRivaroxaban treatment just after MI in Hypo E mice prevented the progression of ICM by attenuating cardiac remodeling, partially through the suppression of the PAR2-mediated inflammatory pathway.

Indexed as

Disease Models, AnimalAnimalsCardiomyopathiesDietDisease ProgressionFactor Xa InhibitorsMaleMiceMice, KnockoutMice, Knockout, ApoEMyocardial InfarctionMyocardial IschemiaRivaroxabanScavenger Receptors, Class BFactor Xa InhibitorsRivaroxabanScarb1 protein, mouseScavenger Receptors, Class BAtherosclerosisCardiac remodelingIschemic cardiomyopathyProtease-activated receptor 2Rivaroxaban

Identifiers

PMID30867376
PMCPMC6800390
OpenAlexW2921702202

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.