ArticleRespiratory research2025
Activation of Nrf2 pathway by 4-Octyl itaconate enhances donor lung function in cold preservation settings.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- Lung transplantation in 2025: a narrative review of progress, challenges, and the road ahead.Journal of thoracic disease · 2026Review
- Exploring the Mechanism of Therapeutic Effects of Polydatin in Lung Ischemia-Reperfusion Injury by Network Pharmacology and Experiment Validation.Journal of inflammation research · 2026Article
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 2026Review
- β-Nicotinamide mononucleotide activates the SIRT1/NF-κB pathway to alleviate ischemia reperfusion injury after lung transplantation.Journal of translational medicine · 2025Article
- Reprogramming immunity with itaconate: metabolic mechanisms and therapeutic perspectives.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundLung transplantation is the primary treatment for end-stage lung diseases. However, ischemia-reperfusion injury (IRI) significantly impacts transplant outcomes. 4-Octyl itaconate (4-OI) has shown potential in mitigating organ IRI, although its effects in lung transplantation require further exploration.
methodsBEAS-2B cells were used to model transplantation, assessing the effects of 4-OI through viability, apoptosis, and ROS assays. qRT-PCR analyzed cytokine transcription post-cold ischemia/reperfusion (CI/R). RNA sequencing and Gene Ontology analysis elucidated 4-OI's mechanisms of action, confirmed by Western blotting. ALI-airway and lung transplantation organoid models evaluated improvements in bronchial epithelial morphology and function due to 4-OI. ELISA measured IL-6 and IL-8 levels. Rat models of extended cold preservation and non-heart-beating transplantation assessed 4-OI's impact on lung function, injury, and inflammation.
resultsOur findings indicate that 4-OI (100 µM) during cold preservation effectively maintained cell viability, decreased apoptosis, and reduced ROS production in BEAS-2B cells under CI/R conditions. It also downregulated pro-inflammatory cytokine transcription, including IL1B, IL6, and TNF. Inhibition of Nrf2 partially reversed these protective effects. In cold preservation solutions, 4-OI upregulated Nrf2 target genes such as NQO1, HMOX1, and SLC7A11. In ALI airway models, 4-OI enhanced bronchial epithelial barrier integrity and ciliary beat function after CI/R. In rat models, 4-OI administration improved lung function and reduced pulmonary edema, tissue injury, apoptosis, and systemic inflammation following extended cold preservation or non-heart-beating lung transplantation.
conclusionsIncorporating 4-OI into cold preservation solutions appears promising for alleviating CI/R-induced bronchial epithelial injury and enhancing lung transplant outcomes via Nrf2 pathway activation.
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