ArticleClinical and experimental nephrology2017
Double inhibition of cAMP and mTOR signalling may potentiate the reduction of cell growth in ADPKD cells.
Article in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Use of mammalian target of rapamycin inhibitors in patient with autosomal dominant polycystic kidney disease: an updated meta-analysis.International urology and nephrology · 2019Pooled it
- Autosomal Dominant Polycystic Kidney Disease: Is There a Role for Autophagy?International journal of molecular sciences · 2023Review
- Plant-derived compounds for treating autosomal dominant polycystic kidney disease.Frontiers in nephrology · 2023Review
- Combination of curcumin and ginkgolide B inhibits cystogenesis by regulating multiple signaling pathways.Molecular medicine reports · 2021Article
- mTOR Signaling in Kidney Diseases.Kidney360 · 2020Review
- The consequences of increased 4E-BP1 in polycystic kidney disease.Human molecular genetics · 2019Article
- Fundamental insights into autosomal dominant polycystic kidney disease from human-based cell models.Pediatric nephrology (Berlin, Germany) · 2019Article
- TRPP2 dysfunction decreases ATP-evoked calcium, induces cell aggregation and stimulates proliferation in T lymphocytes.BMC nephrology · 2019Article
- MicroRNA501-5p induces p53 proteasome degradation through the activation of the mTOR/MDM2 pathway in ADPKD cells.Journal of cellular physiology · 2018Article
- Bilineal inheritance of pathogenic PKD1 and PKD2 variants in a Czech family with autosomal dominant polycystic kidney disease - a case report.BMC nephrology · 2018Article
- Engineered Kidney Tubules for Modeling Patient-Specific Diseases and Drug Discovery.EBioMedicine · 2018Article
- Effects of TORC1 Inhibition during the Early and Established Phases of Polycystic Kidney Disease.PloS one · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundADPKD is a renal pathology caused by mutations of PKD1 and PKD2 genes, which encode for polycystin-1 (PC1) and polycystin-2 (PC2), respectively. PC1 plays an important role regulating several signal transducers, including cAMP and mTOR, which are involved in abnormal cell proliferation of ADPKD cells leading to the development and expansion of kidney cysts that are a typical hallmark of this disease. Therefore, the inhibition of both pathways could potentiate the reduction of cell proliferation enhancing benefits for ADPKD patients.
methodsThe inhibition of cAMP- and mTOR-related signalling was performed by Cl-IB-MECA, an agonist of A3 receptors, and rapamycin, respectively. Protein kinase activity was evaluated by immunoblot and cell growth was analyzed by direct cell counting.
resultsThe activation of A
conclusionThe double treatment with rapamycin and Cl-IB-MECA may have synergistic effects on the inhibition of cell proliferation in ADPKD cells suggesting that combined therapies could improve renal function in ADPKD patients.
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Registered trials
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