ArticleJournal of molecular medicine (Berlin, Germany)2016
Glucose promotes secretion-dependent renal cyst growth.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Progressive endocannabinoid system dysregulation in autosomal dominant polycystic kidney disease.Molecular medicine (Cambridge, Mass.) · 2026Article
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- The Influence of Non-Pharmacological and Pharmacological Interventions on the Course of Autosomal Dominant Polycystic Kidney Disease.Nutrients · 2024Review
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
- Association Between Metabolic Syndrome and the Size of Renal Cysts: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Nonpharmacological Management of Autosomal Dominant Polycystic Kidney Disease.Advances in kidney disease and health · 2023Review
- Role of ANO1 in tumors and tumor immunity.Journal of cancer research and clinical oncology · 2022Review
- Sodium-glucose cotransporter inhibition in polycystic kidney disease: fact or fiction.Clinical kidney journal · 2022Review
- Article
- Metabolic reprogramming in a slowly developing orthologous model of polycystic kidney disease.American journal of physiology. Renal physiology · 2022Article
- The CaActa pharmaceutica Sinica. B · 2021Review
- Macrophage migration inhibitory factor is regulated by HIF-1α and cAMP and promotes renal cyst cell proliferation in a macrophage-independent manner.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Apoptosis and autophagy in polycystic kidney disease (PKD).Cellular signalling · 2020Review
- Ketosis Ameliorates Renal Cyst Growth in Polycystic Kidney Disease.Cell metabolism · 2019Article
- Effect of Trehalose Supplementation on Autophagy and Cystogenesis in a Mouse Model of Polycystic Kidney Disease.Nutrients · 2018Article
- P2Y2R is a direct target of HIF-1α and mediates secretion-dependent cyst growth of renal cyst-forming epithelial cells.Purinergic signalling · 2016Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledPolycystic kidney diseases are characterized by the development of numerous bilateral renal cysts that continuously enlarge resulting in a decline of kidney function due to compression of intact nephrons. Cyst growth is driven by transepithelial chloride secretion which depends on both intracellular cAMP and calcium. Mechanisms that are involved in the regulation of the underlying secretory pathways remain incompletely understood. Here we show that glucose concentration has a strong impact on cyst growth of renal tubular cells within a collagen matrix as well as in embryonic kidneys deficient or competent for Pkd1. Glucose-dependent cyst growth correlates with the transcriptional induction of the calcium-activated chloride channel anoctamin 1 (ANO1) and its increased expression in the apical membrane of cyst-forming cells. Inhibition of ANO1 with the specific inhibitor CaCCinh-AO1 significantly decreases glucose-dependent cyst growth in both models. Ussing chamber analyses revealed increased apical chloride secretion of renal tubular cells upon exposure to high glucose medium which can also be inhibited by the use of CaCCinh-AO1. These data suggest that glycemic control may help to reduce renal cyst growth in patients with polycystic kidney disease. KEY MESSAGE: Renal cyst growth depends on glucose concentration in two in vitro cyst models. High glucose leads to upregulation of the calcium-activated chloride channel ANO1. High glucose promotes calcium-activated chloride secretion via ANO1. Glucose-dependent secretion can be inhibited by a specific inhibitor of ANO1.
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