Evidence map›Paper›PMID 32317079›Full record

ArticleBMB reports2020

GPx7 ameliorates non-alcoholic steatohepatitis by regulating oxidative stress.

Hyeon Ju Kim, Yoseob Lee, Sungsoon Fang, Won Kim, Hyo Jung Kim, Jae-Woo Kim

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Mechanism-centered target discovery across glomerulonephritis phenotypes: an integrative multi-omics study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

6 authors at 2 institutions in 1 country.

Hyeon Ju KimDepartment of Biochemistry and Molecular Biology, Chronic Intractable Disease for Systems Medicine Research Center, Yonsei University College of Medicine, Seoul 03722; Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722, Korea.
Yoseob LeeDepartment of Biochemistry and Molecular Biology, Chronic Intractable Disease for Systems Medicine Research Center, Yonsei University College of Medicine, Seoul 03722; Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722, Korea.
Sungsoon FangBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722; Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Won KimDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul Metropolitan Government Boramae Medical Center, Seoul 07061, Korea.
Hyo Jung Kim1Department of Biochemistry and Molecular Biology, Chronic Intractable Disease for Systems Medicine Research Center, Yonsei University College of Medicine, Seoul 03722, Korea.
Jae-Woo KimDepartment of Biochemistry and Molecular Biology, Chronic Intractable Disease for Systems Medicine Research Center, Yonsei University College of Medicine, Seoul 03722; Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722, Korea.
Yonsei University · KRSeoul Metropolitan Government · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. NAFLD can further progress to irreversible liver failure such as non-alcoholic steatohepatitis (NASH) fibrosis and cirrhosis. However, specific regulator of NASH fibrosis has yet to be established. Here, we found that glutathione peroxidase 7 (GPx7) was markedly expressed in NASH fibrosis. Although GPx7 is an antioxidant enzyme protecting other organs, whether GPx7 plays a role in NASH fibrosis has yet to be studied. We found that knockdown of GPx7 in transforming growth factor-β (TGF-β) and free fatty acids (FFA)-treated LX-2 cells elevated the expression of pro-fibrotic and pro-inflammatory genes and collagen synthesis. Consistently, GPx7 overexpression in LX-2 cells led to the suppression of ROS production and reduced the expression of pro-fibrotic and pro-inflammatory genes. Further, NASH fibrosis induced by choline-deficient amino acid defined, high fat diet (CDAHFD) feeding was significantly accelerated by knockdown of GPx7, as evidenced by up-regulated liver fibrosis and inflammation compared with CDAHFD control mice. Collectively, these results suggest that GPx7 might be a novel therapeutic target to prevent the progression and development of NAFLD. [BMB Reports 2020; 53(6): 317-322].

Indexed as

Oxidative StressAnimalsCarrier ProteinsCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseCarrier ProteinsNPGPx protein, mouse

Identifiers

PMID32317079
PMCPMC7330808
OpenAlexW3016310274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.