Evidence map›Paper›PMID 35194060›Full record

ArticleScientific reports2022

Pemafibrate suppresses NLRP3 inflammasome activation in the liver and heart in a novel mouse model of steatohepatitis-related cardiomyopathy.

Kotaro Kanno, Masahiro Koseki, Jiuyang Chang, Ayami Saga, Hiroyasu Inui, Takeshi Okada, Katsunao Tanaka, Masumi Asaji, Yinghong Zhu, Seiko Ide and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  16. Exploring the alleviating effects ofFrontiers in microbiology · 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

20 authors at 5 institutions in 1 country.

Kotaro KannoDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Masahiro KosekiDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan. koseki@cardiology.med.osaka-u.ac.jp.
Jiuyang ChangDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Ayami SagaDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hiroyasu InuiDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Takeshi OkadaDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Katsunao TanakaDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Masumi AsajiDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yinghong ZhuDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Seiko IdeDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shigeyoshi SaitoDivision of Health Sciences, Department of Medical Physics and Engineering, Osaka University Graduate School of Medicine, Osaka, Japan.
Tomoaki HigoDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Daisuke OkuzakiGenome Information Research Centre, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tohru OhamaDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Makoto NishidaDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yoshihiro KamadaDepartment of Advanced Metabolic Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Masafumi OnoDivision of Innovative Medicine for Hepatobiliary and Pancreatology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Toshiji SaibaraDepartment of Gastroenterology and Hepatology, Kochi Medical School, Kochi, Japan.
Shizuya YamashitaDepartment of Cardiology, Rinku General Medical Centre, Osaka, Japan.
Yasushi SakataDivision of Cardiovascular Medicine, Department of Medicine, Osaka University Graduate School of Medicine, 2-2-B5 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Osaka University · JPOsaka Health Science University · JPKagawa University · JPKochi Medical School Hospital · JPOsaka Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although patients with nonalcoholic fatty liver disease have been reported to have cardiac dysfunction, and appropriate model has not been reported. We established a novel mouse model of diet-induced steatohepatitis-related cardiomyopathy and evaluated the effect of pemafibrate. C57Bl/6 male mice were fed a (1) chow diet (C), (2) high-fat, high-cholesterol, high-sucrose, bile acid diet (NASH diet; N), or (3) N with pemafibrate 0.1 mg/kg (NP) for 8 weeks. In the liver, macrophage infiltration and fibrosis in the liver was observed in the N group compared to the C group, suggesting steatohepatitis. Free cholesterol accumulated, and cholesterol crystals were observed. In the heart, free cholesterol similarly accumulated and concentric hypertrophy was observed. Ultrahigh magnetic field magnetic resonance imaging revealed that the left ventricular (LV) ejection fraction (EF) was attenuated and LV strain was focally impaired. RNA sequencing demonstrated that the NOD-like receptor and PI3 kinase-Akt pathways were enhanced. mRNA and protein expression of inflammasome-related genes, such as Caspase-1, NLRP3, and IL-1β, were upregulated in both the liver and heart. In the NP compared to the N group, steatohepatitis, hepatic steatosis, and cardiac dysfunction were suppressed. Sequential administration of pemafibrate after the development of steatohepatitis-related cardiomyopathy recovered hepatic fibrosis and cardiac dysfunction.

Indexed as

AnimalsBenzoxazolesButyratesCardiomyopathiesDietary CarbohydratesDiet, High-FatDisease Models, AnimalGene ExpressionInflammasomesLiverMaleMiceMice, Inbred C57BLMyocardiumNLR Family, Pyrin Domain-Containing 3 ProteinNon-alcoholic Fatty Liver DiseaseBenzoxazolesButyratesDietary CarbohydratesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouse(R)-2-(3-((benzoxazol-2-yl-d4 (3-(4-methoxyphenoxy-d7)propyl)amino)methyl)phenoxy) butanoic acid

Identifiers

PMID35194060
PMCPMC8863801
OpenAlexW4212988950

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.