Evidence map›Paper›PMID 26442469›Full record

ArticleScientific reports2015

Rhesus monkey model of liver disease reflecting clinical disease progression and hepatic gene expression analysis.

Hong Wang, Tao Tan, Junfeng Wang, Yuyu Niu, Yaping Yan, Xiangyu Guo, Yu Kang, Yanchao Duan, Shaohui Chang, Jianpeng Liao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 24 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Hong WangYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Tao TanYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Junfeng WangDepartment of Hepatobiliary Surgery, The First People's Hospital of Yunnan Province, Kunhua Hospital Affiliated to Kunming Medical College, Kunming, China.
Yuyu NiuYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Yaping YanNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Xiangyu GuoNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Yu KangYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Yanchao DuanNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Shaohui ChangNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Jianpeng LiaoNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Chenyang SiNational Engineering Research Center of Biomedicine and Animal Science, Kunming, Yunnan, China.
Weizhi JiYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Wei SiYunnan Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, Yunnan, Chin.
Kunming University of Science and Technology · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is a significant public health issue with heavy medical and economic burdens. The aetiology of ALD is not yet completely understood. The development of drugs and therapies for ALD is hampered by a lack of suitable animal models that replicate both the histological and metabolic features of human ALD. Here, we characterize a rhesus monkey model of alcohol-induced liver steatosis and hepatic fibrosis that is compatible with the clinical progression of the biochemistry and pathology in humans with ALD. Microarray analysis of hepatic gene expression was conducted to identify potential molecular signatures of ALD progression. The up-regulation of expression of hepatic genes related to liver steatosis (CPT1A, FASN, LEPR, RXRA, IGFBP1, PPARGC1A and SLC2A4) was detected in our rhesus model, as was the down-regulation of such genes (CYP7A1, HMGCR, GCK and PNPLA3) and the up-regulation of expression of hepatic genes related to liver cancer (E2F1, OPCML, FZD7, IGFBP1 and LEF1). Our results demonstrate that this ALD model reflects the clinical disease progression and hepatic gene expression observed in humans. These findings will be useful for increasing the understanding of ALD pathogenesis and will benefit the development of new therapeutic procedures and pharmacological reagents for treating ALD.

Indexed as

Disease Models, AnimalGene Expression ProfilingAnimalsBiomarkersDisease ProgressionEthanolHumansLiver Diseases, AlcoholicMacaca mulattaMicroarray AnalysisBiomarkersEthanol

Identifiers

PMID26442469
PMCPMC4595740
OpenAlexW2408795915

What OpenQuestion holds

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LicenceCC BY
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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.