Evidence map›Paper›PMID 41744810›Full record

ArticleCells2026

Plasma Extracellular Vesicles from Bronchopulmonary Dysplasia Infants Initiate Inflammation and Abnormal Angiogenesis in Neonatal Murine Retinas.

Huijun Yuan, Matthew R Duncan, Shaoyi Chen, Merline Benny, Augusto Schmidt, Karen Young, Audina M Berrocal, M Elizabeth Hartnett, Shu Wu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2026. 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

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

1 citing paper in PubMed.

  1. Article
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.

Huijun YuanDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Matthew R DuncanDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Shaoyi ChenDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Merline BennyDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Augusto SchmidtDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Karen YoungDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Audina M BerrocalBascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, FL33136, USA.
M Elizabeth HartnettByers Eye Institute, Stanford University, Palo Alto, CA 94305, USA.
Shu WuDivision of Neonatology, Department of Pediatrics, Batchelor Children's Research Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.

Funding

Exosomal Gasdermin D Mediated Lung to Brain Crosswalk in Preterm Brain InjuryR01HL156803 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WU, SHU · 2020 to 2023
$2.4M
NIH HHS R01HL156803
6 · The paper itself

Abstract

purposeTo investigate the mechanisms by which plasma extracellular vesicles (EVs) from preterm infants with bronchopulmonary dysplasia (BPD) elicit inflammation and abnormal angiogenesis in neonatal mouse retinas.

methodsEVs from the plasma of 7-day-old preterm infants, born between 23

resultsAdoptively transferred EVs from BPD and nBPD infants crossed the blood-retinal barrier (BRB) in recipient mouse pups. BPD-EVs increased retinal activated microglia, Müller cells, and twisted proliferative neovascularization compared to nBPD-EVs. BPD-EVs also elevated retinal transcripts regulating inflammation and angiogenesis, including NOD-, LRR- and pyrin domain-containing protein 3 (

conclusionsBPD-EVs promote inflammation and abnormal neovascularization by upregulating genes related to apoptosis and inflammation in neonatal mouse retinas. EV protein profiles suggest that elevated levels of proteins such as Defensin alpha 1B (DEFA1B), Insulin-like growth factor binding protein 2 (IGFBP2), CD5 antigen-like (CD5L), von Willebrand factor (vWF), and Tenascin C (TNC) in BPD-EVs may contribute to the observed inflammation and angiogenesis.

Indexed as

BPDextracellular vesiclesneovascularizationretinal inflammationROP

Identifiers

PMID41744810
PMCPMC12940086

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Registered trials

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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.