ArticleFrontiers in immunology2026
CCR1
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease in preterm infants and is characterized by aberrant late-stage lung development driven by multiple factors. Although previous studies have demonstrated that BPD is associated with prenatal and postnatal inflammatory stimuli, the inflammatory mechanisms involved immune cell populations have not been fully elucidated. Here, we systematically investigated the roles of myeloid cells in the inflammatory processes underlying BPD. Using single-cell transcriptomic data of normal and BPD mouse lung, we found that the proportions of several myeloid subpopulations were specifically upregulated in BPD lung, including CCR1
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Registered trials
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.