ArticleThe Journal of thoracic and cardiovascular surgery2024
Mitsugumin 53 mitigation of ischemia-reperfusion injury in a mouse model.
Article in The Journal of thoracic and cardiovascular surgery, 2024. 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, 8 citations in OpenAlex.
- GSK'872 mitigates ischemia-reperfusion injury in rat lung transplants by regulating PANoptosis and inflammation in cell type specific manner.Cell communication and signaling : CCS · 2026Article
- MG53 Coordinates Macrophage Polarization and Neuroimmune Coupling to Promote Corneal Nerve Regeneration via the MPEG1-MVP-STAT6 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitsugumin 53 protects against smoke inhalation lung injury via suppressing the proinflammatory response in a rat model.Free radical biology & medicine · 2026Article
- Improving lung allograft function in the early post-operative period through the inhibition of pyroptosis.Medical review (2021) · 2024Review
- Ex Vivo Lung Perfusion and Primary Graft Dysfunction Following Lung Transplantation: A Contemporary United Network for Organ Sharing Database Analysis.Journal of clinical medicine · 2024Article
- MG53 mitigates warm ischemic lung injury in a murine model of transplantation.The Journal of thoracic and cardiovascular surgery · 2024Article
- MG53/TRIM72: multi-organ repair protein and beyond.Frontiers in physiology · 2024Review
- The Next Frontier in Lung Transplantation: Protecting the Endothelium and Repairing Organs for Transplant Utilizing MG53.Clinical and translational discovery · 2023Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectivePrimary graft dysfunction is often attributed to ischemia-reperfusion injury, and prevention would be a therapeutic approach to mitigate injury. Mitsugumin 53, a myokine, is a component of the endogenous cell membrane repair machinery. Previously, exogenous administration of recombinant human (recombinant human mitsugumin 53) protein has been shown to mitigate acute lung injury. In this study, we aimed to quantify a therapeutic benefit of recombinant human mitsugumin 53 to mitigate a transplant-relevant model of ischemia-reperfusion injury.
methodsC57BL/6J mice were subjected to 1 hour of ischemia (via left lung hilar clamp), followed by 24 hours of reperfusion. mg53
resultsAdministration of recombinant human mitsugumin 53 showed a significant decrease in an established biometric profile of lung injury as measured by lactate dehydrogenase and endothelin-1 in the bronchoalveolar lavage and plasma. Biochemical markers of apoptosis and pyroptosis (interleukin-1β and tumor necrosis factor-α) were also significantly mitigated, overall demonstrating recombinant human mitsugumin 53's ability to decrease the inflammatory response of ischemia-reperfusion injury. Exogenous recombinant human mitsugumin 53 administration showed a trend toward decreasing overall cellular infiltrate and neutrophil response. Fluorescent colocalization imaging revealed recombinant human mitsugumin 53 was effectively delivered to the endothelium.
conclusionsThese data demonstrate that recombinant human mitsugumin 53 has the potential to prevent or reverse ischemia-reperfusion injury-mediated lung damage. Although additional studies are needed in wild-type mice to demonstrate efficacy, this work serves as proof-of-concept to indicate the potential therapeutic benefit of mitsugumin 53 administration to mitigate ischemia-reperfusion injury.
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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.