ReviewAntioxidants (Basel, Switzerland)2022
Oxidative Stress and Ischemia/Reperfusion Injury in Kidney Transplantation: Focus on Ferroptosis, Mitophagy and New Antioxidants.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.
What it found
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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
86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 143 citations in OpenAlex.
- Protective and nephrotoxic effects of emodin in animal models of kidney injury: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Risk factors for delayed graft function in patients with kidney transplantation: a systematic review and meta-analysis.BMJ open · 2025Pooled it
- Current perspectives and trends on the role of mitochondria in renal ischemia-reperfusion injury from 2005 to 2024: a bibliometric analysis and literature review.Frontiers in physiology · 2025Pooled it
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis in colorectal cancer: Molecular mechanisms and regulatory crosstalk with therapeutic prospects (Review).Oncology reports · 2026Review
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- Schisandrin B Attenuates Renal Fibrotic Remodeling in Association with Restoration of a PPARα-Related Tubular Fatty-Acid Oxidation Program.Biomedicines · 2026Article
- The E3 ligase TRIM29 drives renal ischemia-reperfusion injury by targeting DUSP10 for proteasomal degradation.Cell death & disease · 2026Article
- USAG-1 aggravates renal ischemia‒reperfusion injury via promoting GPX4 degradation-induced ferroptosis.Cell death & disease · 2026Article
- The anticancer properties of dexmedetomidine in papillary thyroid cancer and its underlying mechanisms.Scientific reports · 2026Article
- Targeting ATP11B-YAP axis repairs mitochondrial function and inhibits neuronal ferroptosis to attenuate age-related cognitive decline.Signal transduction and targeted therapy · 2026Article
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- Selenoprotein GPX3 regulates NADPH oxidase expression by inhibiting the MAPK signaling pathway and thereby attenuating the inflammatory response in renal ischemia-reperfusion injury.Genes & diseases · 2026Article
- Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026Review
- PINK1 deacetylation by emodin-induced SIRT3 upregulation alleviates acute kidney injury by Inhibition of ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis.Stem cell research & therapy · 2026Article
- Research progress of nanoparticles in the diagnosis and treatment of renal ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Review
- N-acetyl cysteine amide mitigates oxidative stress and apoptosis in a rat model of renal ischemia-reperfusion injury.Scientific reports · 2026Article
- Nephroprotective effects of visnagin through modulation of macrophage polarization, oxidative stress, inflammation and apoptosis in renal I/R injury.Open medicine (Warsaw, Poland) · 2026Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although there has been technical and pharmacological progress in kidney transplant medicine, some patients may experience acute post-transplant complications. Among the mechanisms involved in these conditions, ischemia/reperfusion (I/R) injury may have a primary pathophysiological role since it is one of the leading causes of delayed graft function (DGF), a slow recovery of the renal function with the need for dialysis (generally during the first week after transplantation). DGF has a significant social and economic impact as it is associated with prolonged hospitalization and the development of severe complications (including acute rejection). During I/R injury, oxidative stress plays a major role activating several pathways including ferroptosis, an iron-driven cell death characterized by iron accumulation and excessive lipid peroxidation, and mitophagy, a selective degradation of damaged mitochondria by autophagy. Ferroptosis may contribute to the renal damage, while mitophagy can have a protective role by reducing the release of reactive oxygen species from dysfunctional mitochondria. Deep comprehension of both pathways may offer the possibility of identifying new early diagnostic noninvasive biomarkers of DGF and introducing new clinically employable pharmacological strategies. In this review we summarize all relevant knowledge in this field and discuss current antioxidant pharmacological strategies that could represent, in the next future, potential treatments for I/R injury.
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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.