APOBEC-1 deletion enhances cisplatin-induced acute kidney injury

Cisplatin (CP) induces acute kidney injury (AKI) whereby proximal tubules undergo regulated necrosis. Repair is almost complete after a single dose. We now demonstrate a role for Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (Apobec-1) that is prominently expressed at the interface b...

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Veröffentlicht in:Scientific reports 2023-12, Vol.13 (1), p.22255-22255, Article 22255
Hauptverfasser: Guo, Xiaojia, Blanc, Valerie, Davidson, Nicholas O., Velazquez, Heino, Chen, Tian-min, Moledina, Dennis G., Moeckel, Gilbert W., Safirstein, Robert L., Desir, Gary V.
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Sprache:eng
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Zusammenfassung:Cisplatin (CP) induces acute kidney injury (AKI) whereby proximal tubules undergo regulated necrosis. Repair is almost complete after a single dose. We now demonstrate a role for Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (Apobec-1) that is prominently expressed at the interface between acute and chronic kidney injury (CKD), in the recovery from AKI. Apobec-1 knockout (KO) mice exhibited greater mortality than in wild type (WT) and more severe AKI in both CP- and unilateral ischemia reperfusion (IR) with nephrectomy. Specifically, plasma creatinine (pCr) 2.6 ± 0.70 mg/dL for KO, n = 10 and 0.16 ± 0.02 for WT, n = 6, p 
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-023-49575-3