ArticleKidney international2020
Kidney-intrinsic factors determine the severity of ischemia/reperfusion injury in a mouse model of delayed graft function.
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Early postoperative galectin-3 for risk stratification of delayed graft function after kidney transplantation.Clinical kidney journal · 2026Article
- USAG-1 aggravates renal ischemia‒reperfusion injury via promoting GPX4 degradation-induced ferroptosis.Cell death & disease · 2026Article
- Impact of ischemia duration on MRI-derived perfusion parameters in a mouse kidney transplant model.European radiology experimental · 2026Article
- Can mouse kidney transplant models inform mechanisms of injury and acceptance in clinical kidney transplantation?American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Review
- Inhibition of De Novo Autoantibody Production Attenuates Chronic Antibody-Mediated Rejection of Kidney Allografts Despite Maintenance of High Donor-Specific Antibody Titers.bioRxiv : the preprint server for biology · 2025Article
- Barriers and Opportunities to Increase Utilization of Donor Kidneys After Death Determined by Circulatory Criteria Among Children and Adults: A Narrative Review.Canadian journal of kidney health and disease · 2025Review
- Roles of Akirin1 in early prediction and treatment of graft kidney ischemia‒reperfusion injury.Smart medicine · 2024Article
- Delayed graft function post renal transplantation: a review on animal models and therapeutics.American journal of physiology. Renal physiology · 2023Review
- Toll-Like Receptor 3 mRNA Expression of Peripheral Blood Mononuclear Cells Identifies Kidney Recipients with Potential for Improved Graft Performance.Annals of transplantation · 2023Article
- Beyond UPR: cell-specific roles of ER stress sensor IRE1α in kidney ischemic injury and transplant rejection.Kidney international · 2023Review
- Impaired fatty acid metabolism perpetuates lipotoxicity along the transition to chronic kidney injury.JCI insight · 2022Article
- CLCF1 is up-regulated in renal ischemia reperfusion injury and may associate with FOXO3.Annals of translational medicine · 2022Article
- Cell stress response impairs de novo NAD+ biosynthesis in the kidney.JCI insight · 2022Article
- Prevention of vascular-allograft rejection by protecting the endothelial glycocalyx with immunosuppressive polymers.Nature biomedical engineering · 2021Article
- Recombinant apoptosis inhibitor of macrophage protein reduces delayed graft function in a murine model of kidney transplantation.PloS one · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Delayed graft function due to transplant ischemia/reperfusion injury adversely affects up to 50% of deceased-donor kidney transplant recipients. However, key factors contributing to the severity of ischemia/reperfusion injury remain unclear. Here, using a clinically relevant mouse model of delayed graft function, we demonstrated that donor genetic background and kidney-intrinsic MyD88/Trif-dependent innate immunity were key determinants of delayed graft function. Functional deterioration of kidney grafts directly corresponded with the duration of cold ischemia time. The graft dysfunction became irreversible after cold ischemia time exceeded six hours. When cold ischemia time reached four hours, kidney grafts displayed histological features reflective of delayed graft function seen in clinical kidney transplantation. Notably, kidneys of B6 mice exhibited significantly more severe histological and functional impairment than kidneys of C3H or BALB/c mice, regardless of recipient strains or alloreactivities. Furthermore, allografts of B6 mice also showed an upregulation of IL-6, neutrophil gelatinase-associated lipocalin, and endoplasmic reticulum stress genes, as well as an increased influx of host neutrophils and memory CD8 T-cells. In contrast, donor MyD88/Trif deficiency inhibited neutrophil influx and decreased the expression of IL-6 and endoplasmic reticulum stress genes, along with improved graft function and prolonged allograft survival. Thus, kidney-intrinsic factors involving genetic characteristics and innate immunity serve as critical determinants of the severity of delayed graft function. This preclinical murine model allows for further investigations of the mechanisms underlying delayed graft function.
Indexed as
Identifiers
What OpenQuestion holds
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.