ReviewInternational journal of molecular sciences2024
Ischemia-Reperfusion Injury in Kidney Transplantation: Mechanisms and Potential Therapeutic Targets.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 48 citations in OpenAlex.
- Resveratrol inhibits renal ischemia and reperfusion injury in diabetes via reducing oxidative stress, inflammation, and apoptosis.Renal failure · 2026Article
- A four-gene signature for diagnosis of acute kidney injury following kidney transplantation.Renal failure · 2026Article
- Urologic malignancy in renal transplant recipients: Analysis of OPTN/UNOS data from 2000 to 2022.BMC cancer · 2026Article
- Article
- The anti-interleukin-6 antibody ALD518-P18 mitigates murine kidney ischemia-reperfusion injury.Scientific reports · 2026Article
- USAG-1 aggravates renal ischemia‒reperfusion injury via promoting GPX4 degradation-induced ferroptosis.Cell death & disease · 2026Article
- Early Endothelial Injury in Pancreas Transplantation: Insights from a Prospective Cohort Largely Composed of Simultaneous Pancreas-Kidney Recipients.Medical sciences (Basel, Switzerland) · 2026Article
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- Identification and functional validation of mitochondria-related genes associated with tubular injury in kidney transplantation and ischemia-reperfusion injury.Biology direct · 2026Article
- High-Dose Voclosporin Protects Against Acute Kidney Injury via Regnase-2-Mediated NGAL MRNA Decay.International journal of molecular sciences · 2026Article
- Damage-Associated Molecular Patterns in Perioperative Anesthesia Care: A Clinical Perspective.Anesthesia research · 2026Article
- Identification of ubiquitination-related signature genes for predicting kidney transplant rejection.Scientific reports · 2026Article
- Impact of ischemia duration on MRI-derived perfusion parameters in a mouse kidney transplant model.European radiology experimental · 2026Article
- Interleukin-33 Promotes Neutrophil Extracellular Trap Formation To Aggravate Renal Ischemia-Reperfusion Injury Through ST2/PI3K/Akt and ST2/PAD4 Pathways.Inflammation · 2026Article
- Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system.Frontiers in toxicology · 2026Article
- SEC61: a potential therapeutic target in transplantation.Frontiers in immunology · 2026Review
- Variability and longitudinal dynamics of donor-derived cell-free DNA in kidney and liver recipients: a comparison of absolute and relative quantities in plasma and urine.Frontiers in transplantation · 2026Article
- Nobiletin from Xiaoyu Xiezhuo Decoction: Restoring Mitochondrial Dynamics and Alleviating Renal Ischemia-Reperfusion Injury via M1 Macrophage Modulation.Kidney & blood pressure research · 2026Article
- Article
- Renoprotective mechanisms of bioconverted wild-simulated ginseng: mitigating oxidative stress, inflammation, and apoptosis to protect against ischemic renal injury via Nrf2/HO-1/NF-κB/caspase-3 signaling.Journal of ginseng research · 2026Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidney transplantation offers a longer life expectancy and a better quality of life than dialysis to patients with end-stage kidney disease. Ischemia-reperfusion injury (IRI) is thought to be a cornerstone in delayed or reduced graft function and increases the risk of rejection by triggering the immunogenicity of the organ. IRI is an unavoidable event that happens when the blood supply is temporarily reduced and then restored to an organ. IRI is the result of several biological pathways, such as transcriptional reprogramming, apoptosis and necrosis, innate and adaptive immune responses, and endothelial dysfunction. Tubular cells mostly depend on fatty acid (FA) β-oxidation for energy production since more ATP molecules are yielded per substrate molecule than glucose oxidation. Upon ischemia-reperfusion damage, the innate and adaptive immune system activates to achieve tissue clearance and repair. Several cells, cytokines, enzymes, receptors, and ligands are known to take part in these events. The complement cascade might start even before organ procurement in deceased donors. However, additional experimental and clinical data are required to better understand the pathogenic events that take place during this complex process.
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Registered trials
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