Evidence map›Paper›PMID 40715658›Full record

ArticleNature immunology2025

Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.

Yohei Abe, Nathanael J Spann, Wenxi Tang, Fenghua Zeng, Cadence Seymour, Sean Jansky, Jason L Guo, Robert Huff, Kelly Chanthavixay, John Lalith Charles Richard and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Reconceptualizing chorioamnionitis as an immune-mediated inflammatory disorder at the maternal-fetal interface.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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

18 authors.

Yohei AbeDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.
Nathanael J SpannDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.
Wenxi TangDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Fenghua ZengDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Cadence SeymourDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Sean JanskyDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Jason L GuoHagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Robert HuffDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Kelly ChanthavixayDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
John Lalith Charles RichardDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Miguel MooneyDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA.
Debanjan DharDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Souradipta GangulyDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
David M LopezHagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0009-0002-3116-0253
Michael T LongakerHagey Laboratory for Pediatric Regenerative Medicine, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Christopher BennerDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Christopher K GlassDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA. ckg@ucsd.edu.ORCID http://orcid.org/0000-0003-4344-3592
Eniko SajtiDepartment of Pediatrics, University of California San Diego, La Jolla, CA, USA. esajti@health.ucsd.edu.ORCID http://orcid.org/0000-0002-0531-7715

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Role of neonatal lung macrophages in mediating resilience to hyperoxia induced lung injury via TREM2 signalingR01HL170183 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Eniko Sajti · 2023 to 2026
$3.0M
Illumina NovaSeq 6000 Sequencing SystemS10OD026929 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JEPSEN, KRISTEN LYNN · 2019 to 2019
$600k
Spatiotemporal Atlas of Cellular Networks and Ultrastructural States Mediating the Progression and Resolution of Pulmonary FibrosisF32HL167318 · NHLBI · STANFORD UNIVERSITY · PI GUO, JASON LIWEI · 2023 to 2024
$146k
American Heart Association (American Heart Association, Inc.) 23PRE1025458MEXT | Japan Society for the Promotion of Science (JSPS) 201860150NCI NIH HHS P30 CA023100NHLBI NIH HHS F32 HL167318NHLBI NIH HHS R01 HL170183NIH HHS S10 OD026929U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01- HL170183A
6 · The paper itself

Abstract

Bronchopulmonary dysplasia is a common complication of preterm birth, driven in part by the inflammatory effects of supplemental oxygen on the immature lung. Although oxygen therapy is essential, it contributes to disrupted lung development but not all infants are equally susceptible. Using genetically diverse mouse models, we found that hyperoxia-sensitive mice exhibit a distinct innate immune response compared to resilient strains. Notably, the hyperoxia-sensitive C57BL/6J strain showed selective upregulation of TREM2 on lung macrophages and monocytes. Deletion of TREM2 in myeloid cells led to reduced inflammation, preserved alveolar structure and sustained cell proliferation in the developing lung following oxygen exposure. Mechanistically, TREM2 loss limited p53 activation, favoring cell-cycle arrest over apoptosis. These results identify TREM2 as a key driver of immune-mediated lung injury in neonatal hyperoxia and suggest it may be a promising therapeutic target for preventing or treating bronchopulmonary dysplasia in vulnerable preterm infants.

Indexed as

Bronchopulmonary DysplasiaHyperoxiaLung InjuryMembrane GlycoproteinsOxygenReceptors, ImmunologicTumor Suppressor Protein p53AnimalsAnimals, NewbornDisease Models, AnimalGenetic VariationHumansImmunity, InnateLungMiceMice, Inbred C57BLMembrane GlycoproteinsOxygenReceptors, ImmunologicTrem2 protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID40715658
PMCPMC12456008

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.