ArticleAnesthesiology2012
Alveolar macrophages and Toll-like receptor 4 mediate ventilated lung ischemia reperfusion injury in mice.
Article in Anesthesiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Dietary tryptophan mitigates lung ischemia-reperfusion injury in association with increased indole-3-propionate and aryl hydrocarbon receptor signaling.Gut microbes · 2026Article
- Gut microbiome-derived propionate reprograms alveolar macrophages metabolically and regulates lung injury responses in mice.Gut microbes · 2026Article
- Design, Synthesis, and Characterization of Prodrugs of Sulfonamide TLR4 Signaling Inhibitor TAK-242 (Resatorvid).ACS medicinal chemistry letters · 2026Article
- Functional remodeling of iNKT cells by sulfatide-reactive type II NKT cells reprograms alveolar macrophages to alleviate lung ischemia-reperfusion injury.Communications biology · 2026Article
- Potential role of ferroptosis in sterile acute lung injury induced by a non-hypoxic ischemia-reperfusion insult.Iranian journal of basic medical sciences · 2026Article
- Gut Microbiota-Derived Lipopolysaccharides and Short-Chain Fatty Acids Regulate Immune Responses via FFAR2/FFAR3 in Lung Ischemia-Reperfusion Injury.Annals of the New York Academy of Sciences · 2025Article
- A mouse model of lung ischemia-reperfusion injury with reversible left hilar entrapment.Animal models and experimental medicine · 2025Article
- Primary Graft Dysfunction in Lung Transplantation: An Overview of the Molecular Mechanisms.International journal of molecular sciences · 2025Review
- Macrophage regulated cell death: implications and mechanisms in organ transplantation.Frontiers in immunology · 2025Review
- Cathepsin C from extracellular histone-induced M1 alveolar macrophages promotes NETosis during lung ischemia-reperfusion injury.Redox biology · 2024Article
- High Dose of Estrogen Protects the Lungs from Ischemia-Reperfusion Injury by Downregulating the Angiotensin II Signaling Pathway.Inflammation · 2024Article
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Hemopexin alleviates sterile inflammation in ischemia-reperfusion-induced lung injury.Frontiers in immunology · 2024Article
- Sulfonamide Prodrugs with a Two-Stage Release Mechanism for the Efficient Delivery of the TLR4 Antagonist TAK-242.ACS medicinal chemistry letters · 2023Article
- Immune response associated with ischemia and reperfusion injury during organ transplantation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- A Mouse Model of Orotracheal Intubation and Ventilated Lung Ischemia Reperfusion Surgery.Journal of visualized experiments : JoVE · 2022Article
- Baicalin relievesMolecular medicine reports · 2021Article
- WISP1 and TLR4 on Macrophages Contribute to Ventilator-Induced Lung Injury.Inflammation · 2020Article
- Elevated Gut Microbiome-Derived Propionate Levels Are Associated With Reduced Sterile Lung Inflammation and Bacterial Immunity in Mice.Frontiers in microbiology · 2019Article
- Pathophysiology and classification of primary graft dysfunction after lung transplantation.Journal of thoracic disease · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIschemia-reperfusion (I-R) injury is a sterile inflammatory process that is commonly associated with diverse clinical situations such as hemorrhage followed by resuscitation, transient embolic events, and organ transplantation. I-R injury can induce lung dysfunction whether the I-R occurs in the lung or in a remote organ. Recently, evidence has emerged that receptors and pathways of the innate immune system are involved in recognizing sterile inflammation and overlap considerably with those involved in the recognition of and response to pathogens.
methodsThe authors used a mouse surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. In addition, they mimicked nutritional I-R injury in vitro by transiently depriving cells of all nutrients.
resultsCompared with sham-operated mice, mice subjected to ventilated lung I-R injury had up-regulated lung expression of inflammatory mediator messenger RNA for interleukin-1β, interleukin-6, and chemokine (C-X-C motif) ligand-1 and -2, paralleled by histologic evidence of lung neutrophil recruitment and increased plasma concentrations of interleukin-1β, interleukin-6, and high-mobility group protein B1 proteins. This inflammatory response to I-R required toll-like receptor-4 (TLR4). In addition, the authors demonstrated in vitro cooperativity and cross-talk between human macrophages and endothelial cells, resulting in augmented inflammatory responses to I-R. Remarkably, the authors found that selective depletion of alveolar macrophages rendered mice resistant to ventilated lung I-R injury.
conclusionsThe data reveal that alveolar macrophages and the pattern recognition receptor toll-like receptor-4 are involved in the generation of the early inflammatory response to lung I-R injury.
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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.