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Profile of gene expression in experimental acute kidney injury

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NIAID Data Ecosystem2026-05-02 收录
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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE273063
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Treatment for acute kidney injury (AKI) is suboptimal. A better understanding of its pathogenesis may lead to new therapeutic approaches. Kidney transcriptomics analyses of murine folic acid-induced AKI (FA-AKI) will allow us to identify new mediators and therapeutic targets of this pathology. Folic acid nephropathy is a classical model of AKI characterized by acute renal failure, tubular cell death, interstitial leukocyte infiltration and subsequent tubular regeneration that has been reported in humans. C57BL/6 female mice received a single intraperitoneal injection of folic acid (Sigma-Aldrich, Merck Darmstadt, Germany) 250 mg/kg in 0.3 mol/L sodium bicarbonate or vehicle (n=3 per group). Mice were euthanized at 24h
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2024-07-30
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