ArticleFrontiers in immunology2024
Transient heat stress protects from severe endothelial damage and dysfunction during prolonged experimental ex-vivo lung perfusion.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Biomarkers of standard criteria and marginal donor lungs during ex vivo lung perfusion: A comparative study.JHLT open · 2026Article
- Progress in Designing Cytokine Antagonist Antibodies for Cancer Therapy.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- From Molecules to Meaning: Integrating Neuropeptides, Sociostasis, and Hormesis in the Brain-Heart Axis.Current issues in molecular biology · 2026Review
- ProlongedFrontiers in transplantation · 2026Article
- Engineering Neutrophil Vesicles for Synergistic Protection against Ischemia/Reperfusion Injury after Lung Transplant.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Systematic production of human kidney organoids for transplantation in porcine kidneys during ex vivo machine perfusion.Nature biomedical engineering · 2025Article
- Article
- Lipid metabolism-related genes regulate the immune microenvironment during ex vivo lung perfusion for lung transplants.Journal of thoracic disease · 2025Article
- Optimal duration of ex vivo lung perfusion for heat stress-mediated therapeutic reconditioning of damaged rat donor lungs.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2025Article
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Authors and funding
7 authors.
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Abstract
Introduction: The pulmonary endothelium is the primary target of lung ischemia-reperfusion injury leading to primary graft dysfunction after lung transplantation. We hypothesized that treating damaged rat lungs by a transient heat stress during ex-vivo lung perfusion (EVLP) to elicit a pulmonary heat shock response could protect the endothelium from severe reperfusion injury. Methods: Rat lungs damaged by 1h warm ischemia were reperfused on an EVLP platform for up to 6h at a constant temperature (T°) of 37°C (EVLP Results: HS induced an early (3h) and persisting expression of HSP70 and HSP27, without influencing Hsc70. Lungs from the EVLP Conclusion: The therapeutic application of a transient heat stress during EVLP of damaged rat lungs reduces endothelial permeability, attenuates pulmonary vasoconstriction, prevents src-kinase activation and VE-cadherin phosphorylation, while reducing endothelial peroxinitrite generation and the release of cytokines and endothelial biomarkers. Collectively, these data demonstrate that therapeutic heat stress may represent a promising strategy to protect the lung endothelium from severe reperfusion injury.
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