ReviewInternational journal of molecular sciences2023
Acute Kidney Injury by Ischemia/Reperfusion and Extracellular Vesicles.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 53 citations in OpenAlex.
- Potential targets and molecular mechanisms of D-pinitol against acute kidney injury based on network pharmacology and experimental validation.Renal failure · 2026Article
- Sigma-1 receptor protects against renal ischemia-reperfusion injury by enhancing mitophagy via Rac1 regulation.Renal failure · 2026Article
- Salvianolic acid C alleviates acute kidney injury by restoring fructose-1,6-bisphosphatase 1-mediated gluconeogenesis.Renal failure · 2026Article
- Transcriptome and weighted gene co-expression network analysis identify hub genes and pathways in rat kidneys after deep hypothermic circulatory arrest.Renal failure · 2026Article
- Targeting biglycan-TLR2/TLR4 interaction with synthetic peptides mitigates inflammation and ameliorates renal function in ischemia-reperfusion injury.Cellular & molecular biology letters · 2026Article
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting HMGB1 for Renal Ischemia and Reperfusion Injury: Mechanisms and Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- Alpha-Mangostin in Acute Kidney Injury: Molecular Mechanisms, Regulated Cell Death, and Translational Opportunities.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Integrative Network Pharmacology and Molecular Docking Analysis Uncovers Multi-Target Mechanisms of Alpha-Mangostin Against Acute Kidney Injury.Foods (Basel, Switzerland) · 2026Article
- Renoprotective Potential of Nateglinide in an Acute Kidney Injury Model.International journal of molecular sciences · 2026Article
- The role of interleukin-4 in acute kidney injury and chronic kidney disease: a literature review.BMC nephrology · 2026Review
- Research progress of nanoparticles in the diagnosis and treatment of renal ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Review
- Therapeutic effect of Yupingfeng powder and its bioactive metabolites on renal diseases.Frontiers in pharmacology · 2026Review
- Predictive value of Index of Cardiac Electrophysiological Balance (ICEB) for ischemia-reperfusion injury following coronary artery angioplasty.American journal of translational research · 2026Article
- The Current Application Prospects of Nanomedicine in Renal Ischemia-Reperfusion Injury.International journal of nanomedicine · 2026Review
- Plant metabolites: potential treatments for ischemic acute kidney injury.Frontiers in pharmacology · 2026Review
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Integration of transcriptome and Mendelian randomization analyses in exploring the extracellular vesicle-related biomarkers of diabetic kidney disease.Renal failure · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute kidney injury (AKI) is often caused by ischemia-reperfusion injury (IRI). IRI significantly affects kidney metabolism, which elicits pro-inflammatory responses and kidney injury. The ischemia/reperfusion of the kidney is associated with transient high mitochondrial-derived reactive oxygen species (ROS) production rates. Excessive mitochondrial-derived ROS damages cellular components and, together with other pathogenic mechanisms, elicits a range of acute injury mechanisms that impair kidney function. Mitochondrial-derived ROS production also stimulates epithelial cell secretion of extracellular vesicles (EVs) containing RNAs, lipids, and proteins, suggesting that EVs are involved in AKI pathogenesis. This literature review focuses on how EV secretion is stimulated during ischemia/reperfusion and how cell-specific EVs and their molecular cargo may modify the IRI process. Moreover, critical pitfalls in the analysis of kidney epithelial-derived EVs are described. In particular, we will focus on how the release of kidney epithelial EVs is affected during tissue analyses and how this may confound data on cell-to-cell signaling. By increasing awareness of methodological pitfalls in renal EV research, the risk of false negatives can be mitigated. This will improve future EV data interpretation regarding EVs contribution to AKI pathogenesis and their potential as biomarkers or treatments for AKI.
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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 Socratic graph.