ArticleScientific reports2019
A mouse model of renal fibrosis to overcome the technical variability in ischaemia/reperfusion injury among operators.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
- Renoprotective Effects of MIT-001 in Ischemia-Reperfusion Injury: Modulation of Ferroptosis, ROS and Fibrotic Markers.Journal of cellular and molecular medicine · 2025Article
- Aptamer-targeted anti-miR RNA construct based on 3WJ as a new approach for the treatment of chronic kidney disease in an experimental model.Gene therapy · 2025Article
- Kidney Fibrosis In Vitro and In Vivo Models: Path Toward Physiologically Relevant Humanized Models.Advanced healthcare materials · 2025Review
- Development of a Model of Tubulointerstitial Fibrosis Using Transient Unilateral Renal Ischemia and Delayed Contralateral Nephrectomy in Domesticated Cats.Comparative medicine · 2024Article
- Pharmacological and Pathological Effects of Mulberry Leaf Extract on the Treatment of Type 1 Diabetes Mellitus Mice.Current issues in molecular biology · 2023Article
- T CellAntioxidants & redox signaling · 2023Article
- ZEB2 controls kidney stromal progenitor differentiation and inhibits abnormal myofibroblast expansion and kidney fibrosis.JCI insight · 2023Article
- Causal effects of human serum metabolites on occurrence and progress indicators of chronic kidney disease: a two-sample Mendelian randomization study.Frontiers in nutrition · 2023Article
- Effects of contralateral nephrectomy timing and ischemic conditions on kidney fibrosis after unilateral kidney ischemia-reperfusion injury.Renal failure · 2022Article
- Mesenchymal Stem Cell-Derived Exosomes: Toward Cell-Free Therapeutic Strategies in Chronic Kidney Disease.Frontiers in medicine · 2022Review
- Protease-Activated Receptor 1 Contributes to Microcirculation Failure and Tubular Damage in Renal Ischemia-Reperfusion Injury in Mice.BioMed research international · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ischaemia-reperfusion (I/R) model is a widely used model of acute kidney injury (AKI) and renal fibrosis. However, the ischaemia duration that is long enough to cause broad fibrosis shows that a high mortality rate and a short ischaemia duration does not cause fibrosis, resulting in a large variation in fibrosis progression in this experimental model. Inter-operator variation occurs for I/R injury severity because the I/R procedure is complex, which results in poor reproducibility of subsequent fibrosis in the model. In the present study, we developed a renal fibrosis model in which the fibrosis progression for 8 weeks is predictable within 8 days. Three operators independently performed I/R followed by uninephrectomy at day 7 in mice. The aim was to create a model that would show a blood urea nitrogen (BUN) level >100 mg/dL at day 8 after I/R (day 1 after uninephrectomy). Although the ischaemia duration to satisfy this BUN criterion differed among operators, the mice developed anaemia, polyuria, and fibrosis in a similar manner under the same BUN criterion with a low mortality rate. Interstitial fibrosis had developed at week 8, which was strongly correlated with the BUN at day 8. This protocol allows operators to adjust the ischaemia duration based on the BUN criterion and to separate mice into the desired number of groups based on the BUN to study interventions against renal fibrosis.
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