ArticleJournal of biomedical science2020
"Point of no return" in unilateral renal ischemia reperfusion injury in mice.
Article in Journal of biomedical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- [Risk factors for perioperative acute kidney injury following partial nephrectomy in patients with stage 3 chronic kidney disease].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- Sodium bicarbonate attenuates myocardial ischemia-reperfusion injury via activation of the splenic cholinergic anti-inflammatory pathway.JTCVS open · 2026Article
- Quantification of Kidney Inflammation Using Nanobubble-mediated Contrast Enhanced Ultrasound.Nanotheranostics · 2026Article
- Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From acute tubular injury to tubular repair and chronic kidney diseases - KIM-1 as a promising biomarker for predicting renal tubular pathology.Current research in physiology · 2025Review
- Chronic central nervous system leptin administration attenuates kidney dysfunction and injury in a model of ischemia/reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Sexually dimorphic renal expression of mouse Klotho is directed by a kidney-specific distal enhancer responsive to HNF1b.Communications biology · 2024Article
- Prevention of Transition from Acute Kidney Injury to Chronic Kidney Disease Using Clinical-Grade Perinatal Stem Cells in Non-Clinical Study.International journal of molecular sciences · 2024Article
- In vitro study of the embolic characteristics of imipenem/cilastatin particles.CVIR endovascular · 2024Article
- Mitigative role of cysteamine against unilateral renal reperfusion injury in Wistar rats.Frontiers in pharmacology · 2024Article
- Targeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis.Journal of translational medicine · 2023Article
- IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells.Cellular and molecular life sciences : CMLS · 2023Article
- Enhancing the expression of a key mitochondrial enzyme at the inception of ischemia-reperfusion injury can boost recovery and halt the progression of acute kidney injury.Frontiers in physiology · 2023Article
- Transcriptome analysis of renal ischemia/reperfusion (I/R) injury in BAFF and BAFF-R deficient mice.PloS one · 2023Article
- Analysis of mRNA and protein kidney injury Molecule-1 (KIM-1) expression in a kidney model during the initiation phase of ischemia reperfusion injury.Annals of medicine and surgery (2012) · 2022Article
- Combined Systemic Intake of K-ATP Opener (Nicorandil) and Mesenchymal Stem Cells Preconditioned With Nicorandil Alleviates Pancreatic Insufficiency in a Model of Bilateral Renal Ischemia/Reperfusion Injury.Frontiers in physiology · 2022Article
- Angiotensin type 2 receptor activation limits kidney injury during the early phase and induces Treg cells during the late phase of renal ischemia.American journal of physiology. Renal physiology · 2021Article
- Intravital imaging of real-time endogenous actin dysregulation in proximal and distal tubules at the onset of severe ischemia-reperfusion injury.Scientific reports · 2021Article
- Integrated Analysis of the CircRNA-Based ceRNA Network in Renal Fibrosis Induced by Ischemia Reperfusion Injury.Frontiers in genetics · 2021Article
- Revealing the Angiopathy of Lacrimal Gland Lesion in Type 2 Diabetes.Frontiers in physiology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIn the past years evidence has been growing about the interconnection of chronic kidney disease and acute kidney injury. The underlying pathophysiological mechanisms remain unclear. We hypothesized, that a threshold ischemia time in unilateral ischemia/reperfusion injury sets an extent of ischemic tubule necrosis, which as "point of no return" leads to progressive injury. This progress is temporarily associated by increased markers of inflammation and results in fibrosis and atrophy of the ischemic kidney.
methodsAcute tubule necrosis was induced by unilateral ischemia/reperfusion injury in male C57BL/6 N mice with different ischemia times (15, 25, 35, and 45 min). At multiple time points between 15 min and 5 weeks we assessed gene expression of markers for injury, inflammation, and fibrosis, histologically the injury of tubules, cell death (TUNEL), macrophages, neutrophil influx and kidney atrophy.
resultsUnilateral ischemia for 15 and 25 min induced upregulation of markers for injury after reperfusion for 24 h but no upregulation after 5 weeks. None of the markers for inflammation or fibrosis were upregulated after ischemia for 15 and 25 min at 24 h or 5 weeks on a gene expression level, except for Il-6. Ischemia for 35 and 45 min consistently induced upregulation of markers for inflammation, injury, and partially of fibrosis (Tgf-β1 and Col1a1) at 24 h and 5 weeks. The threshold ischemia time for persistent injury of 35 min induced a temporal association of markers for inflammation and injury with peaks between 6 h and 7 d along the course of 10 d. This ischemia time also induced persistent cell death (TUNEL) throughout observation for 5 weeks with a peak at 6 h and progressing kidney atrophy beginning 7 d after ischemia.
conclusionsThis study confirms the evidence of a threshold extent of ischemic injury in which markers of injury, inflammation and fibrosis do not decline to baseline but remain upregulated assessed in long term outcome (5 weeks). Excess of this threshold as "point of no return" leads to persistent cell death and progressing atrophy and is characterized by a temporal association of markers for inflammation and injury.
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