ArticlePloS one2013
Ischemia-reperfusion lung injury is attenuated in MyD88-deficient mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Inflammatory Myeloid Cell Resurgence and Impaired Pro-Resolution Macrophage Maintenance Characterize Chronic Corneal Alkali Burn.Investigative ophthalmology & visual science · 2026Article
- CD11b suppresses TLR activation of nonclassical monocytes to reduce primary graft dysfunction after lung transplantation.The Journal of clinical investigation · 2022Article
- Innate immunity in lung transplantation.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021Review
- Sterile inflammation in thoracic transplantation.Cellular and molecular life sciences : CMLS · 2021Review
- Effect of Intravenous Lidocaine on Inflammatory and Apoptotic Response of Ischemia-Reperfusion Injury in Pigs Undergoing Lung Resection Surgery.BioMed research international · 2021Article
- Anti-inflammatory action of cysteine derivative S-1-propenylcysteine by inducing MyD88 degradation.Scientific reports · 2018Article
- The innate immune response to ischemic injury: a multiscale modeling perspective.BMC systems biology · 2018Article
- Ferulic acid exerts neuroprotective effects against cerebral ischemia/reperfusion-induced injury via antioxidant and anti-apoptotic mechanisms in vitro and in vivo.International journal of molecular medicine · 2017Article
- Models of Lung Transplant Research: a consensus statement from the National Heart, Lung, and Blood Institute workshop.JCI insight · 2017Review
- Mechanisms of graft rejection after lung transplantation.Current opinion in organ transplantation · 2017Review
- Beneficial effect of low-level laser therapy in acute lung injury after i-I/R is dependent on the secretion of IL-10 and independent of the TLR/MyD88 signaling.Lasers in medical science · 2017Article
- Perioperative "remote" acute lung injury: recent update.Journal of biomedical research · 2017Article
- Article
- Ischaemic and inflammatory injury in renal graft from brain death donation: an update review.Journal of anesthesia · 2016Review
- Primary ciliary dyskinesia.Seminars in respiratory and critical care medicine · 2015Review
- Human recombinant apyrase therapy protects against canine pulmonary ischemia-reperfusion injury.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2015Article
- The TIR-domain-containing adapter inducing interferon-β-dependent signaling cascade plays a crucial role in ischemia-reperfusion-induced retinal injury, whereas the contribution of the myeloid differentiation primary response 88-dependent signaling cascade is not as pivotal.The European journal of neuroscience · 2014Article
- Human myocardium releases heat shock protein 27 (HSP27) after global ischemia: the proinflammatory effect of extracellular HSP27 through toll-like receptor (TLR)-2 and TLR4.Molecular medicine (Cambridge, Mass.) · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Ischemia-reperfusion lung injury is a common cause of acute morbidity and mortality in lung transplant recipients and has been associated with subsequent development of bronchiolitis obliterans syndrome. Recognition of endogenous ligands released during cellular injury (damage-associated molecular patterns; DAMPs) by Toll-like receptors (TLRs), especially TLR4, has increasingly been recognized as a mechanism for inflammation resulting from tissue damage. TLR4 is implicated in the pathogenesis of ischemia-reperfusion injury of multiple organs including heart, liver, kidney and lung. Additionally, activation of TLRs other than TLR4 by DAMPs has been identified in tissues other than the lung. Because all known TLRs, with the exception of TLR3, signal via the MyD88 adapter protein, we hypothesized that lung ischemia-reperfusion injury was mediated by MyD88-dependent signaling. To test this hypothesis, we subjected C57BL/6 wildtype, Myd88(-/-), and Tlr4(-/-) mice to 1 hr of left lung warm ischemia followed by 4 hr of reperfusion. We found that Myd88(-/-) mice had significantly less MCP-1/CCL2 in the left lung following ischemia-reperfusion as compared with wildtype mice. This difference was associated with dramatically reduced lung permeability. Interestingly, Tlr4(-/-) mice had only partial protection from ischemia-reperfusion as compared to Myd88(-/-) mice, implicating other MyD88-dependent pathways in lung injury following ischemia-reperfusion. We also found that left lung ischemia-reperfusion caused remote inflammation in the right lung. Finally, using chimeric mice with MyD88 expression restricted to either myeloid or non-myeloid cells, we found that MyD88-dependent signaling in myeloid cells was necessary for ischemia-reperfusion induced lung permeability. We conclude that MyD88-dependent signaling through multiple receptors is important in the pathogenesis of acute lung inflammation and injury following ischemia and reperfusion.
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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.