Evidence map›Paper›PMID 34193972›Full record

ArticleCommunications biology2021

Auranofin prevents liver fibrosis by system Xc-mediated inhibition of NLRP3 inflammasome.

Hyun Young Kim, Young Jae Choi, Sang Kyum Kim, Hyunsung Kim, Dae Won Jun, Kyungrok Yoon, Nayoun Kim, Jungwook Hwang, Young-Mi Kim, Sung Chul Lim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 30 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

11 authors at 4 institutions in 2 countries.

Hyun Young KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Young Jae ChoiCollege of Pharmacy, Chungnam National University, Daejeon, Republic of Korea.
Sang Kyum KimCollege of Pharmacy, Chungnam National University, Daejeon, Republic of Korea.
Hyunsung KimDepartment of Pathology, Hanyang University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-8935-7414
Dae Won JunDepartment of Internal Medicine, Hanyang University College of Medicine, Seoul, Republic of Korea.ORCID 0000-0002-2875-6139
Kyungrok YoonCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Nayoun KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea.
Jungwook HwangGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Republic of Korea.ORCID 0000-0002-2290-1649
Young-Mi KimCollege of Pharmacy and Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, Gyeonggi-do, Republic of Korea.
Sung Chul LimCollege of Medicine, Chosun University, Gwangju, Republic of Korea.
Keon Wook KangCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, Republic of Korea. kwkang@snu.ac.kr.ORCID 0000-0003-2867-8940
Seoul National University · KRHanyang University · KRChungnam National University · KRChosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Demand for a cure of liver fibrosis is rising with its increasing morbidity and mortality. Therefore, it is an urgent issue to investigate its therapeutic candidates. Liver fibrosis progresses following 'multi-hit' processes involving hepatic stellate cells, macrophages, and hepatocytes. The NOD-like receptor protein 3 (NLRP3) inflammasome is emerging as a therapeutic target in liver fibrosis. Previous studies showed that the anti-rheumatic agent auranofin inhibits the NLRP3 inflammasome; thus, this study evaluates the antifibrotic effect of auranofin in vivo and explores the underlying molecular mechanism. The antifibrotic effect of auranofin is assessed in thioacetamide- and carbon tetrachloride-induced liver fibrosis models. Moreover, hepatic stellate cell (HSC), bone marrow-derived macrophage (BMDM), kupffer cell, and hepatocyte are used to examine the underlying mechanism of auranofin. Auranofin potently inhibits activation of the NLRP3 inflammasome in BMDM and kupffer cell. It also reduces the migration of HSC. The underlying molecular mechanism was inhibition of cystine-glutamate antiporter, system Xc. Auranofin inhibits system Xc activity and instantly induced oxidative burst, which mediated inhibition of the NLRP3 inflammasome in macrophages and HSCs. Therefore, to the best of our knowledge, we propose the use of auranofin as an anti-liver fibrotic agent.

Indexed as

Amino Acid Transport System y+AnimalsApoptosisAuranofinCarbon TetrachlorideCells, CulturedHumansInflammasomesInterleukin-1betaKupffer CellsLiverLiver CirrhosisMacrophagesMaleMiceMice, Inbred BALB CAmino Acid Transport System y+AuranofinCarbon TetrachlorideInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinThioacetamide

Identifiers

PMID34193972
PMCPMC8245406
OpenAlexW3173879725

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.