ArticleCell death discovery2025
IL-1β
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Small intracellular vesicle-liposome fusogenic nanoplatform sIVs-LPs@Hes: Nebulized delivery targeting pulmonary inflammatory microenvironment to improve ALI.Materials today. Bio · 2026Article
- Ultrasensitive detection of lung inflammation in male mice using immuno-magnetic particle imaging.Nature communications · 2026Article
- Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution.Frontiers in immunology · 2026Review
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Matrine Alleviates Sepsis-Induced Acute Lung Injury by Reinforcing NQO1/SLC7A11/GPX4-Associated Anti-Ferroptotic Defenses and Attenuating NF-κB-Driven Inflammation.Drug design, development and therapy · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute lung injury (ALI) involves a complex interplay between immune cells and the pulmonary endothelium. However, the molecular regulators that coordinate this interaction remain poorly defined. In a murine sepsis model, we identified a subset of lung-resident macrophages characterized by robust IL-1β expression as pivotal contributors to lung damage. Single-cell RNA sequencing (scRNA-seq) delineated a distinct IL-1β⁺ macrophage population with pronounced pro-inflammatory transcriptional features and enhanced endothelial communication. These macrophages exhibited intensified ligand-receptor interactions with pulmonary endothelial cells, corresponding with elevated vascular leakage and histopathological evidence of injury. Immunoassays, Western blotting, and histopathology confirmed IL-1β upregulation during lung injury. Furthermore, metabolomics and in vitro co-culture experiments demonstrated that IL-1β impairs endothelial integrity and modulates metabolic activity. This study reveals a novel immune-metabolic axis whereby IL-1β
Identifiers
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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.