ArticleKidney international2013
Chromosome substitution modulates resistance to ischemia reperfusion injury in Brown Norway rats.
Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Engineering polyamidoamine dendrimer nanoparticles for targeted drug delivery to proximal tubular cells after renal ischemia/reperfusion injury.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- The role of sex and gender in acute kidney injury-consensus statements from the 33rd Acute Disease Quality Initiative.Kidney international · 2025Article
- Sulfotransferase 1C2 Increases Mitochondrial Respiration by Converting Mitochondrial Membrane Cholesterol to Cholesterol Sulfate.Biochemistry · 2024Article
- Role of actin cytoskeleton in podocytes.Pediatric nephrology (Berlin, Germany) · 2021Review
- Specific Lowering of Asymmetric Dimethylarginine by Pharmacological Dimethylarginine Dimethylaminohydrolase Improves Endothelial Function, Reduces Blood Pressure and Ischemia-Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2021Article
- Mutation of RORγT reveals a role for Th17 cells in both injury and recovery from renal ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2020Article
- Long-term outcomes in mouse models of ischemia-reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2019Article
- Endothelial prostacyclin protects the kidney from ischemia-reperfusion injury.Pflugers Archiv : European journal of physiology · 2019Article
- Hydrodynamic Isotonic Fluid Delivery Ameliorates Moderate-to-Severe Ischemia-Reperfusion Injury in Rat Kidneys.Journal of the American Society of Nephrology : JASN · 2017Article
- Endothelial colony-forming cells ameliorate endothelial dysfunction via secreted factors following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2017Article
- Bridging translation for acute kidney injury with better preclinical modeling of human disease.American journal of physiology. Renal physiology · 2016Review
- AKI and Genetics: Evolving Concepts in the Genetics of Acute Kidney Injury: Implications for Pediatric AKI.Journal of pediatric genetics · 2016Review
- Macrophage-derived Lipocalin-2 contributes to ischemic resistance mechanisms by protecting from renal injury.Scientific reports · 2016Article
- Deficiency in the Formation of 20-Hydroxyeicosatetraenoic Acid Enhances Renal Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Brown Norway rats (BN, BN/NHsdMcwi) are profoundly resistant to developing acute kidney injury (AKI) following ischemia reperfusion. To help define the genetic basis for this resistance, we used consomic rats, in which individual chromosomes from BN rats were placed into the genetic background of Dahl SS rats (SS, SS/JrHsdMcwi) to determine which chromosomes contain alleles contributing to protection from AKI. The parental strains had dramatically different sensitivity to ischemia reperfusion with plasma creatinine levels following 45 min of ischemia and 24 h reperfusion of 4.1 and 1.3 mg/dl in SS and BN, respectively. No consomic strain showed protection similar to the parental BN strain. Nine consomic strains (SS-7(BN), SS-X(BN), SS-8(BN), SS-4(BN), SS-15(BN), SS-3(BN), SS-10(BN), SS-6(BN), and SS-5(BN)) showed partial protection (plasma creatinine about 2.5-3.0 mg/dl), suggesting that multiple alleles contribute to the severity of AKI. In silico analysis was performed using disease ontology database terms and renal function quantitative trait loci from the Rat Genome Database on the BN chromosomes giving partial protection from AKI. This tactic identified at least 36 candidate genes, with several previously linked to the pathophysiology of AKI. Thus, natural variants of these alleles or yet-to-be identified alleles on these chromosomes provide protection against AKI. These alleles may be potential modulators of AKI in susceptible patient populations.
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