ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Combination siRNA delivery as a therapeutic strategy for ADPKD.bioRxiv : the preprint server for biology · 2026Article
- Toward Physiologically Relevant Organoid Models of Polycystic Kidney Disease through Microenvironment Reconstruction.Journal of the American Society of Nephrology : JASN · 2026Review
- The CLCA1/TMEM16A/Cl- current axis associates with H2S deficiency in diabetic kidney injury.JCI insight · 2025Article
- GLPG2737, a CFTR Inhibitor, Prevents Cyst Growth in Preclinical Models of Autosomal Dominant Polycystic Kidney Disease.American journal of nephrology · 2025Article
- Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).Journal of cellular signaling · 2025Article
- Multiscale and multimodal evaluation of autosomal dominant polycystic kidney disease development.Communications biology · 2024Article
- Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.International journal of molecular sciences · 2023Review
- Calcium signaling in polycystic kidney disease- cell death and survival.Cell calcium · 2023Review
- Article
- Physiology assays in human kidney organoids.American journal of physiology. Renal physiology · 2022Review
- Emerging therapies for autosomal dominant polycystic kidney disease with a focus on cAMP signaling.Frontiers in molecular biosciences · 2022Review
- The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the development of bilateral renal cysts which enlarge continuously, leading to compression of adjacent intact nephrons. The growing cysts lead to a progressive decline in renal function. Cyst growth is driven by enhanced cell proliferation and chloride secretion into the cyst lumen. Chloride secretion is believed to occur mainly by the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR), with some contribution by the calcium-activated chloride channel TMEM16A. However, our previous work suggested TMEM16A as a major factor for renal cyst formation. The contribution of CFTR to cyst formation has never been demonstrated in an adult ADPKD mouse model. We used mice with an inducible tubule-specific Pkd1 knockout, which consistently develop polycystic kidneys upon deletion of Pkd1. Cellular properties, ion currents, and cyst development in these mice were compared with that of mice carrying a co-deletion of Pkd1 and Cftr. Knockout of Cftr did not reveal any significant impact on cyst formation in the ADPKD mouse model. Furthermore, knockout of Cftr did not attenuate the largely augmented cell proliferation observed in Pkd1 knockout kidneys. Patch clamp analysis on primary renal epithelial cells lacking expression of Pkd1 indicated an only marginal contribution of CFTR to whole cell Cl
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