Evidence map›Paper›PMID 39060815›Full record

ArticleInflammation2025

PAI-1 Deficiency Promotes NET-mediated Pyroptosis and Ferroptosis during Pseudomonas Aeruginosa-induced Acute Lung Injury by Regulating the PI3K/MAPK/AKT Axis.

Nurbiya Aji, Linlin Wang, Sijiao Wang, Ting Pan, Juan Song, Cuicui Chen, Lu Wang, Nana Feng, Xinjun Tang, Yuanlin Song

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. SERPINE1 in ARDS: an emerging regulator of inflammation-coagulation-fibrinolysis crosstalk.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Article
  5. Article
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  7. Article
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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

10 authors.

Nurbiya AjiShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Linlin WangShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Sijiao WangShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ting PanShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Juan SongShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Cuicui ChenShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Lu Wang
Nana FengDepartment of Respiratory and Critical Medicine, Shanghai Eighth People's Hospital Affiliated to Jiangsu University, Shanghai, China. fnn2005508@126.com.
Xinjun TangShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China. tangxj0531@126.com.
Yuanlin SongShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary and Critical Medicine Zhongshan Hospital, Fudan University, Shanghai, 200032, China. song.yuanlin@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circulating neutrophil extracellular trap (NET) formation is an adaptive process during acute lung injury (ALI). The important role of plasminogen activator inhibitor (PAI)-1 in NET formation during ALI remains unclear. This research intends to examine the impacts of the decrease in PAI-1 levels on NET formation and the underlying mechanism. We found a relative association between the increase in plasma NET levels and thromboinflammation-induced lung damage in patients with ARDS. PAI-1 knockout (KO) mice exhibited significant increases in Pseudomonas aeruginosa (PAO1 strain)-induced ALI, inflammation, inflammatory cell accumulation, and proinflammatory cytokine secretion, and wild-type mice exhibited the opposite changes. During PAO1-induced ALI, PAI-1 KO increased NET release and the levels of prothrombotic markers in mice. PAI-1 deficiency also promoted NET formation and NET-mediated pyroptosis and ferroptosis by activating the PI3K/MAPK/AKT pathway in a PAO1-induced ALI mouse model. In conclusion, PAI-1 KO exacerbated PAO1-induced pneumonia-associated injury and contributed to NET-mediated pyroptosis and ferroptosis through PI3K/MAPK/AKT pathway activation. Thus, targeting PAI-1 and NETs may be a promising therapeutic approach for ameliorating pneumonia and thromboinflammation-associated ALI.

Indexed as

Acute Lung InjuryExtracellular TrapsFerroptosisPlasminogen Activator Inhibitor 1Pseudomonas aeruginosaPseudomonas InfectionsPyroptosisAnimalsHumansMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPhosphatidylinositol 3-KinasesPlasminogen Activator Inhibitor 1Proto-Oncogene Proteins c-aktferroptosisInflammationneutrophil extracellular trapsplasminogen activator inhibitor-1pyroptosis

Identifiers

PMID39060815

What Socratic holds

Textmetadata
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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 Socratic graph.