Evidence map›Paper›PMID 41316369›Full record

ArticleEuropean journal of medical research2025

Sestrin2 ameliorates LPS-induced cardiomyocyte injury by inhibiting ferroptosis via the Nrf2/HO-1 pathway.

Yiheng Yang, Peng Yang, Zhenzhong Zheng, Qingshan Tian

Abstract read
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Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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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

4 authors.

Yiheng YangDepartment of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
Peng YangDepartment of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
Zhenzhong ZhengDepartment of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China. greateful@163.com.
Qingshan TianDepartment of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China. ndyfy10093@ncu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathogenesis of sepsis-induced myocardial injury is complex. Currently, treatment for this disease remains suboptimal. Sestrin2 (Sesn2) is an antioxidant protein and has been shown to have a protective role in some diseases. However, its role in sepsis-induced cardiomyocyte injury has not been fully elucidated.

methodsAn in vitro model of sepsis-induced myocardial injury was established by treating H9c2 cardiomyocytes with lipopolysaccharide (LPS). The viability of H9c2 cardiomyocytes was quantified using the cell counting kit-8. Protein expression levels were analyzed by Western blotting. Apoptosis and mitochondrial membrane potential were quantified by flow cytometry. Mitochondrial ultrastructure was observed by transmission electron microscopy. Malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), reactive oxygen species (ROS), and iron content were quantified using commercial assay kits. The ferroptosis inducer Erastin was employed to further investigate the role of Sesn2 in ferroptosis. The potential regulatory relationship between Sesn2 and the Nrf2/HO-1 pathway was investigated using the Nrf2 inhibitor ML385.

resultsSesn2 overexpression significantly improved cell viability, ameliorated mitochondrial damage, upregulated GPX4 and SLC7A11 expression, downregulated ACSL4 expression, reduced MDA and Fe

conclusionsThis study demonstrates that Sesn2 inhibits ferroptosis in LPS-treated H9c2 cells through the Nrf2/HO-1 pathway, and also exerts an anti-apoptotic effect.

Indexed as

FerroptosisHeme Oxygenase-1Myocytes, CardiacNF-E2-Related Factor 2Nuclear ProteinsAnimalsApoptosisCell LineHeme Oxygenase (Decyclizing)LipopolysaccharidesRatsReactive Oxygen SpeciesSepsisSestrinsSignal TransductionHeme Oxygenase-1Heme Oxygenase (Decyclizing)Hmox1 protein, ratLipopolysaccharidesNfe2l2 protein, ratNF-E2-Related Factor 2Nuclear ProteinsReactive Oxygen SpeciesSesn2 protein, ratSestrinsFerroptosisLPSNrf2/HO-1Sepsis-induced myocardial injurySestrin2

Identifiers

PMID41316369
PMCPMC12764043

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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.