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PF-06409577 通过同时抑制 mTOR 通路和 CFTR 通道活性来抑制肾脏囊肿的进展。

PF-06409577 inhibits renal cyst progression by concurrently inhibiting the mTOR pathway and CFTR channel activity.

机构信息

Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, China.

Department of Urology, The Affiliated Hospital of Xuzhou Medical University, China.

出版信息

FEBS Open Bio. 2022 Oct;12(10):1761-1770. doi: 10.1002/2211-5463.13459. Epub 2022 Jul 4.

Abstract

Renal cyst development and expansion in autosomal dominant polycystic kidney disease (ADPKD) involves over-proliferation of cyst-lining epithelial cells and excessive cystic fluid secretion. While metformin effectively inhibits renal cyst growth in mouse models of ADPKD it exhibits low potency, and thus an adenosine monophosphate-activated protein kinase (AMPK) activator with higher potency is required. Herein, we adopted a drug repurposing strategy to explore the potential of PF-06409577, an AMPK activator for diabetic nephropathy, in cellular, ex vivo and in vivo models of ADPKD. Our results demonstrated that PF-06409577 effectively down-regulated mammalian target of rapamycin pathway-mediated proliferation of cyst-lining epithelial cells and reduced cystic fibrosis transmembrane conductance regulator-regulated cystic fluid secretion. Overall, our data suggest that PF-06409577 holds therapeutic potential for ADPKD treatment.

摘要

常染色体显性多囊肾病(ADPKD)中肾囊肿的发生和扩张涉及囊衬上皮细胞的过度增殖和囊性液体分泌过多。二甲双胍能有效抑制 ADPKD 小鼠模型的肾囊肿生长,但作用效力较低,因此需要一种作用效力更高的腺苷单磷酸激活蛋白激酶(AMPK)激活剂。在此,我们采用药物再利用策略,探索 AMPK 激活剂 PF-06409577 对 ADPKD 的细胞、离体和体内模型的潜在疗效。结果表明,PF-06409577 能有效下调雷帕霉素靶蛋白通路介导的囊衬上皮细胞增殖,并减少囊性纤维化跨膜电导调节子调控的囊性液体分泌。总之,我们的数据表明 PF-06409577 具有治疗 ADPKD 的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de01/9527591/cd328c08f317/FEB4-12-1761-g002.jpg

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