Evidence map›Paper›PMID 37946128›Full record

ArticleCellular & molecular biology letters2023

Irf7 regulates the expression of Srg3 and ferroptosis axis aggravated sepsis-induced acute lung injury.

Xinyu Ling, Shiyou Wei, Dandan Ling, Siqi Cao, Rui Chang, Qiuyun Wang, Zhize Yuan

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
13.4field-weighted citation impact, top 1% 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

31 citing papers in PubMed, 52 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

7 authors at 4 institutions in 1 country.

Xinyu Ling *Department of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, 200433, China.
Shiyou Wei *Department of Anesthesiology, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, 200433, China.
Dandan LingDepartment of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Siqi CaoSchool of Clinical Medicine, Weifang Medical University, Weifang, 261053, Shandong, China.
Rui ChangMedical Department, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, 200433, China.
Qiuyun WangDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. drwangqiuyun@126.com.
Zhize YuanDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai, 200433, China. yuanzhize0402@tongji.edu.cn.ORCID http://orcid.org/0000-0003-3633-6860
Tongji University · CNFudan University Shanghai Cancer Center · CNRuijin Hospital · CNWeifang Medical University · CN

Funding

Shanghai Sailing program 21YF1408000The National Natural Science Foundation of China 82200285The National Natural Science Foundation of China 82202362
6 · The paper itself

Abstract

objectiveTo investigate the mechanism of action of Srg3 in acute lung injury caused by sepsis.

methodsFirst, a sepsis-induced acute lung injury rat model was established using cecal ligation and puncture (CLP). RNA sequencing (RNA-seq) was used to screen for highly expressed genes in sepsis-induced acute lung injury (ALI), and the results showed that Srg3 was significantly upregulated. Then, SWI3-related gene 3 (Srg3) was knocked down using AAV9 vector in vivo, and changes in ALI symptoms in rats were analyzed. In vitro experiments were conducted by establishing a cell model using lipopolysaccharide (LPS)-induced BEAS-2B cells and coculturing them with phorbol 12-myristate 13-acetate (PMA)-treated THP-1 cells to analyze macrophage polarization. Next, downstream signaling pathways regulated by Srg3 and transcription factors involved in regulating Srg3 expression were analyzed using the KEGG database. Finally, gain-of-loss functional validation experiments were performed to analyze the role of downstream signaling pathways regulated by Srg3 and transcription factors involved in regulating Srg3 expression in sepsis-induced acute lung injury.

resultsSrg3 was significantly upregulated in sepsis-induced acute lung injury, and knocking down Srg3 significantly improved the symptoms of ALI in rats. Furthermore, in vitro experiments showed that knocking down Srg3 significantly weakened the inhibitory effect of LPS on the viability of BEAS-2B cells and promoted alternative activation phenotype (M2) macrophage polarization. Subsequent experiments showed that Srg3 can regulate the activation of the NF-κB signaling pathway and promote ferroptosis. Specific activation of the NF-κB signaling pathway or ferroptosis significantly weakened the effect of Srg3 knockdown. It was then found that Srg3 can be transcriptionally activated by interferon regulatory factor 7 (Irf7), and specific inhibition of Irf7 significantly improved the symptoms of ALI.

conclusionsIrf7 transcriptionally activates the expression of Srg3, which can promote ferroptosis and activate classical activation phenotype (M1) macrophage polarization by regulating the NF-κB signaling pathway, thereby exacerbating the symptoms of septic lung injury.

Indexed as

Acute Lung InjuryFerroptosisSepsisAnimalsInterferon Regulatory Factor-7LipopolysaccharidesNF-kappa BRatsTranscription FactorsInterferon Regulatory Factor-7LipopolysaccharidesNF-kappa BTranscription FactorsFerroptosisIrf7NF-κB signaling pathwaySepsis-induced acute lung injurySrg3

Identifiers

PMID37946128
PMCPMC10634032
OpenAlexW4388534490

What OpenQuestion holds

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LicenceCC BY
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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.