PF-06409577 inhibits renal cyst progression by concurrently inhibiting the mTOR pathway and CFTR channel activity.
Limin SuHaoxing YuanHaoran ZhangRuoqi WangKequan FuLong YinYing RenHongli LiuQian FangJunqi WangDong GuoPublished in: FEBS open bio (2022)
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.
Keyphrases
- polycystic kidney disease
- cystic fibrosis
- protein kinase
- diabetic nephropathy
- signaling pathway
- transcription factor
- pseudomonas aeruginosa
- emergency department
- cell proliferation
- lung function
- electronic health record
- chronic obstructive pulmonary disease
- machine learning
- combination therapy
- inflammatory response
- human health
- physical activity