Evidence map›Paper›PMID 38517050›Full record

ArticleClinical and experimental immunology2024

Neutrophil extracellular traps induce pyroptosis of pulmonary microvascular endothelial cells by activating the NLRP3 inflammasome.

Peipei Zhao, Jiarui Zhu, Ling Bai, Wenlan Ma, Feifei Li, Cen Zhang, Liangtao Zhao, Liuyang Wang, Sigong Zhang

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  7. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
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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

9 authors at 1 institution in 1 country.

Peipei ZhaoDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Jiarui ZhuCui Ying Biomedical Research Center, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Ling BaiDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Wenlan MaDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Feifei LiDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Cen ZhangDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Liangtao ZhaoCui Ying Biomedical Research Center, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Liuyang WangDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.
Sigong ZhangDepartment of Rheumatology, Lanzhou University Second Hospital, Lanzhou, Gansu, China.ORCID 0000-0003-1565-1431
Lanzhou University Second Hospital · CN

Funding

National Natural Science Foundation of China 82060302
6 · The paper itself

Abstract

Excessive formation of neutrophil extracellular traps (NETs) may lead to myositis-related interstitial lung disease (ILD). There is evidence that NETs can directly injure vascular endothelial cells and play a pathogenic role in the inflammatory exudation of ILD. However, the specific mechanism is unclear. This study aimed to investigate the specific mechanism underlying NET-induced injury to human pulmonary microvascular endothelial cells (HPMECs). HPMECs were stimulated with NETs (200 ng/ml) in vitro. Cell death was detected by propidium iodide staining. The morphological changes of the cells were observed by transmission electron microscopy (TEM). Pyroptosis markers were detected by western blot, immunofluorescence, and quantitative real-time polymerase chain reaction, and the related inflammatory factor Interleukin-1β (IL-1β) was verified by enzyme-linked immunosorbent assay (ELISA). Compared with the control group, HPMECs mortality increased after NET stimulation, and the number of pyroptosis vacuoles in HPMECs was further observed by TEM. The pulmonary microvascular endothelial cells (PMECs) of the experimental autoimmune myositis mouse model also showed a trend of pyroptosis in vivo. Cell experiment further confirmed the significantly high expression of the NLRP3 inflammasome and pyroptosis-related markers, including GSDMD and inflammatory factor IL-1β. Pretreated with the NLRP3 inhibitor MCC950, the activation of NLRP3 inflammasome and pyroptosis of HPMECs were effectively inhibited. Our study confirmed that NETs promote pulmonary microvascular endothelial pyroptosis by activating the NLRP3 inflammasome, suggesting that NETs-induced pyroptosis of PMECs may be a potential pathogenic mechanism of inflammatory exudation in ILD.

Indexed as

Endothelial CellsExtracellular TrapsInflammasomesLungNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisAnimalsCells, CulturedHumansInterleukin-1betaMiceMice, Inbred C57BLMicrovesselsNeutrophilsInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humaninterstitial lung diseaseneutrophil extracellular trapsNLRP3 inflammasomepulmonary microvascular endothelial cellpyroptosis

Identifiers

PMID38517050
PMCPMC11188539
OpenAlexW4393071671

What Socratic holds

Textmetadata
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 Socratic graph.