Evidence map›Paper›PMID 31847346›Full record

ArticleJournal of clinical medicine2019

Erastin Inhibits Septic Shock and Inflammatory Gene Expression via Suppression of the NF-κB Pathway.

Byung Moo Oh, Seon-Jin Lee, Gyoung Lim Park, Yo Sep Hwang, Jeewon Lim, Eun Sun Park, Kyung Ho Lee, Bo Yeon Kim, Yong Tae Kwon, Hee Jun Cho and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Epigenetic mechanism of HDAC5 in sepsis-induced acute intestinal injury through KLF4-mediated intestinal epithelial cell ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  11. Inflammation in a ferroptotic environment.Frontiers in pharmacology · 2024
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  13. Molecular mechanisms of ferroptosis and relevance to inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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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 3 institutions in 1 country.

Byung Moo OhImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Seon-Jin LeeEnvironmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Gyoung Lim ParkEnvironmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Yo Sep HwangImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Jeewon LimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Eun Sun ParkImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Kyung Ho LeeAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Korea.
Bo Yeon KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Korea.
Yong Tae KwonProtein Metabolism Medical Research Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 110-799, Korea.
Hee Jun ChoImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Hee Gu LeeImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Yuseong-gu, Daejeon 34141, Korea.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KRSeoul National University · KR

Funding

National Research Foundation of Korea 2017R1A2B2005629R&D Convergence Program CAP-16-03-KRIBB
6 · The paper itself

Abstract

Sepsis is a life-threatening condition that is caused by an abnormal immune response to infection and can lead to tissue damage, organ failure, and death. Erastin is a small molecule capable of initiating ferroptotic cell death in cancer cells. However, the function of erastin in the inflammatory response during sepsis remains unknown. Here, we showed that erastin ameliorates septic shock induced by cecal ligation and puncture or lipopolysaccharides (LPS) in mice, which was associated with a reduced production of inflammatory mediators such as nitric oxide, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β. Pretreatment with erastin in bone marrow-derived macrophages (BMDMs) significantly attenuated the expression of inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-1β mRNA in response to LPS treatment. Furthermore, we also showed that erastin suppresses phosphorylation of IκB kinase β, phosphorylation and degradation of IκBα, and nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in LPS-stimulated BMDMs. Our findings suggest that erastin attenuates the inflammatory response by suppressing the NF-κB signaling pathway, resulting in inhibition of sepsis development. This study provides new insights regarding the potential therapeutic properties of erastin in sepsis.

Indexed as

erastinferroptosisinflammationNF-κBsepsis

Identifiers

PMID31847346
PMCPMC6947339
OpenAlexW2995361758

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.