Evidence map›Paper›PMID 35730208›Full record

ArticleClinical and molecular hepatology2022

Auranofin attenuates hepatic steatosis and fibrosis in nonalcoholic fatty liver disease via NRF2 and NF- κB signaling pathways.

Seung Min Lee, Dong Hee Koh, Dae Won Jun, Yoon Jin Roh, Hyeon Tae Kang, Ju Hee Oh, Hyun Sung Kim

Open access · goldAbstract read
In one paragraph

Article in Clinical and molecular hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Seung Min LeeDepartment of Translational Medicine, Graduate School of Biomedical Science & Engineering, Hanyang University, Seoul, Korea.
Dong Hee KohDepartment of Internal Medicine, Hallym University Dongtan Sacred Heart Hospital, Hwaseong, Korea.
Dae Won JunDepartment of Translational Medicine, Graduate School of Biomedical Science & Engineering, Hanyang University, Seoul, Korea.
Yoon Jin RohDepartment of Dermatology, Chung-Ang University Hospital, Seoul, Korea.
Hyeon Tae KangCellivery R&D Institute, Cellivery Therapeutics, Inc., Seoul, Korea.
Ju Hee OhDepartment of Translational Medicine, Graduate School of Biomedical Science & Engineering, Hanyang University, Seoul, Korea.
Hyun Sung KimDepartment of pathology, Hanyang University College of Medicine, Seoul, Korea.
Hanyang University · KRChung-Ang University Hospital · KRHallym University Dongtan Sacred Heart Hospital · KRHanyang University Seoul Hospital · KR

Funding

Hanyang University HY-2017National Research Foundation of Korea 2020R1A2C2009227
6 · The paper itself

Abstract

BACKGROUND/

aimsWe aim to evaluate the effects of auranofin, a known antioxidant, on hepatic steatosis, inflammation, and fibrosis, contributing to non-alcoholic steatohepatitis (NASH) development in vivo and in vitro.

methodsTranscriptome analysis of LX-2 cells was that expression patterns of genes changed by auranofin, and their related pathways were estimated. We used the gene set enrichment analysis (GSEA) program to determine the pathway involved in overall genetic change. In vitro, LX-2 and HepG2 cells were treated with transforming growth factor (TGF)-β1 and palmitic acid (PA), respectively, and the antifibrotic and antiadipogenic effect function of auranofin was evaluated.

resultsTranscriptome analysis revealed that auranofin decreased the expression of 15 genes, including thrombospondin 1, endothelin 1 (ET-1), fibronectin 1, and LOX. The molecular functions of these genes are involved in collagen binding. GSEA of the overall gene expression pattern revealed that many genes increased in the reactive oxygen species pathway and decreased in the inflammatory response. Auranofin decreased nuclear factor kappa B (NF-κB) and IκBα in TGF-β1-induced LX-2 cells, thereby reducing ET-1 and fibrosis. Furthermore, increased pNRF2 in PA-induced HepG2 cells led to increased antioxidant marker expression and decreased lipid accumulation. In the bile duct ligation model mice, auranofin reduced the fibrosis area and increased the survival rate. Auranofin reduced liver fibrosis and lipid accumulation in NASH model mice fed on a Western diet.

conclusionAuranofin inhibits lipogenesis and fibrosis formation and is a proposed candidate for NASH treatment.

Indexed as

Non-alcoholic Fatty Liver DiseaseAnimalsAntioxidantsAuranofinCollagenEndothelin-1FibronectinsHumansLiverLiver CirrhosisMiceMice, Inbred C57BLNF-E2-Related Factor 2NF-kappa BNF-KappaB Inhibitor alphaPalmitic AcidAntioxidantsAuranofinCollagenEndothelin-1FibronectinsNF-E2-Related Factor 2NF-kappa BNF-KappaB Inhibitor alphaPalmitic AcidReactive Oxygen SpeciesThrombospondin 1Transforming Growth Factor beta1Transforming Growth FactorsAntioxidantsAuranofinHepatic fibrosisLipid accumulationNonalcoholic fatty liver disease

Identifiers

PMID35730208
PMCPMC9597229
OpenAlexW4283312208

What OpenQuestion holds

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LicenceCC BY-NC
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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.