Title : AMP-activated protein kinase contributes to cisplatin-induced renal epithelial cell apoptosis and acute kidney injury.

Pub. Date : 2020 Dec 1

PMID : 33103444






5 Functional Relationships(s)
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1 In this study, we demonstrated that cisplatin activates AMPK (Thr172 phosphorylation) in cultured renal tubular epithelial cells in a time-dependent manner, which is associated with p53 phosphorylation. Cisplatin transformation related protein 53, pseudogene Mus musculus
2 Compound C, a selective AMPK inhibitor, suppressed cisplatin-induced AMPK activation, p53 phosphorylation, Bax induction and caspase 3 activation. Cisplatin transformation related protein 53, pseudogene Mus musculus
3 Furthermore, silencing AMPK expression by siRNA attenuated cisplatin-induced p53 phosphorylation, Bax induction, and caspase 3 activation. Cisplatin transformation related protein 53, pseudogene Mus musculus
4 In a mouse model of cisplatin-induced kidney injury, compound C inhibited p53 phosphorylation, Bax expression, caspase 3 activation, and apoptosis, protecting the kidney from injury and dysfunction. Cisplatin transformation related protein 53, pseudogene Mus musculus
5 Taken together, these results suggest that AMPK-p53-Bax signaling pathway plays a crucial role in cisplatin-induced tubular epithelial cell apoptosis. Cisplatin transformation related protein 53, pseudogene Mus musculus