Evidence map›Paper›PMID 26728457›Full record

ArticleThe Journal of biological chemistry2016

Alterations of Hepatic Metabolism in Chronic Kidney Disease via D-box-binding Protein Aggravate the Renal Dysfunction.

Kengo Hamamura, Naoya Matsunaga, Eriko Ikeda, Hideaki Kondo, Hisako Ikeyama, Kazutaka Tokushige, Kazufumi Itcho, Yoko Furuichi, Yuya Yoshida, Masaki Matsuda and 8 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Circadian regulation of renal function.Free radical biology & medicine · 2018
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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

18 authors at 5 institutions in 1 country.

Kengo HamamuraFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan, the Drug Innovation Research Center, Daiichi University of Pharmacy, Minami-ku, Fukuoka 815-8511, Japan.
Naoya MatsunagaFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Eriko IkedaFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan, the Drug Innovation Research Center, Daiichi University of Pharmacy, Minami-ku, Fukuoka 815-8511, Japan.
Hideaki Kondothe Center for Sleep Medicine, Saiseikai Nagasaki Hospital, Katafuchi, Nagasaki 850-0003, Japan.
Hisako IkeyamaFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Kazutaka TokushigeFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Kazufumi ItchoFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Yoko FuruichiFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Yuya YoshidaFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Masaki MatsudaFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Kaori YasudaCell-Innovator Inc., EC Building, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Atsushi DoiCell-Innovator Inc., EC Building, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Yoshifumi Yokotathe Department of Molecular Genetics, School of Medicine, Fukui University, Matsuoka, Fukui 910-1193, Japan.
Toshiaki AmamotoNeues Corporation, Tenyamachi-cho, Hakata-ku, Fukuoka 812-0025, Japan, and.
Hironori Aramakithe Drug Innovation Research Center, Daiichi University of Pharmacy, Minami-ku, Fukuoka 815-8511, Japan, the Department of Molecular Biology, Daiichi University of Pharmacy, Minami-ku, Fukuoka 815-8511, Japan.
Yasuhiro Irinothe Integrated Center for Mass Spectrometry, Division of Membrane Biology, and Department of Evidence-based Laboratory Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Hyogo 650-0017, Japan.
Satoru KoyanagiFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan.
Shigehiro OhdoFrom the Department of Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8512, Japan, ohdo@phar.kyushu-u.ac.jp.
Kyushu University · JPDaiichi University of Pharmacy · JPKobe University · JPNagasaki Ajisai Hospital · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is associated with an increase in serum retinol; however, the underlying mechanisms of this disorder are poorly characterized. Here, we found that the alteration of hepatic metabolism induced the accumulation of serum retinol in 5/6 nephrectomy (5/6Nx) mice. The liver is the major organ responsible for retinol metabolism; accordingly, microarray analysis revealed that the hepatic expression of most CYP genes was changed in 5/6Nx mice. In addition, D-box-binding protein (DBP), which controls the expression of several CYP genes, was significantly decreased in these mice. Cyp3a11 and Cyp26a1, encoding key proteins in retinol metabolism, showed the greatest decrease in expression in 5/6Nx mice, a process mediated by the decreased expression of DBP. Furthermore, an increase of plasma transforming growth factor-β1 (TGF-β1) in 5/6Nx mice led to the decreased expression of the Dbp gene. Consistent with these findings, the alterations of retinol metabolism and renal dysfunction in 5/6Nx mice were ameliorated by administration of an anti-TGF-β1 antibody. We also show that the accumulation of serum retinol induced renal apoptosis in 5/6Nx mice fed a normal diet, whereas renal dysfunction was reduced in mice fed a retinol-free diet. These findings indicate that constitutive Dbp expression plays an important role in mediating hepatic dysfunction under CKD. Thus, the aggravation of renal dysfunction in patients with CKD might be prevented by a recovery of hepatic function, potentially through therapies targeting DBP and retinol.

Indexed as

AnimalsApoptosisCells, CulturedCytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemDNA-Binding ProteinsLiverMaleMembrane ProteinsMiceMice, Inbred ICRRenal Insufficiency, ChronicRetinoic Acid 4-HydroxylaseTranscription FactorsTransforming Growth Factor beta1Vitamin ACyp26a1 protein, mouseCyp3a11 protein, mouseCytochrome P-450 CYP3ACytochrome P-450 Enzyme SystemDbp protein, mouseDNA-Binding ProteinsMembrane ProteinsRetinoic Acid 4-HydroxylaseTranscription FactorsTransforming Growth Factor beta1Vitamin Acircadian clockhepatocyterenal physiologyretinoltransforming growth factor beta (TGF-beta)

Identifiers

PMID26728457
PMCPMC4777830
OpenAlexW2233579919

What OpenQuestion holds

Textmetadata
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.