ReviewAdvances in kidney disease and health2023
Mechanisms of Cyst Development in Polycystic Kidney Disease.
Review in Advances in kidney disease and health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- RhoA through its various effectors mediate mitochondrial fragmentation in polycystic kidney disease.iScience · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- A new conceptual framework for PKD1 in ADPKD; integrating DNA structures and inflammation.BMC nephrology · 2026Review
- Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- AbioRxiv : the preprint server for biology · 2026Article
- ADPKD Progression by Variant Type and Molecular Domain Among Participants in the HALT PKD Trial.Clinical journal of the American Society of Nephrology : CJASN · 2025Article
- Mechanisms of Cyst Expansion in Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Autosomal Dominant Polycystic Kidney Disease Inflammation Biomarkers in the Tolvaptan Era.International journal of molecular sciences · 2025Review
- G-quadruplex stabilization provokes DNA breaks in human PKD1, revealing a second hit mechanism for ADPKD.Nature communications · 2025Article
- Concomitant Wilms tumor and autosomal dominant polycystic kidney disease.Pediatric blood & cancer · 2024Article
- STING Promotes the Progression of ADPKD by Regulating Mitochondrial Function, Inflammation, Fibrosis, and Apoptosis.Biomolecules · 2024Article
- End-stage ADPKD with a low-frequency PKD1 mosaic variant accelerated by chemoradiotherapy.Human genome variation · 2024Article
- HumanmicroPublication biology · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Autosomal dominant polycystic kidney disease is the most common inherited cause of end-stage kidney disease worldwide. Most cases result from mutation of either of 2 genes, PKD1 and PKD2, which encode proteins that form a probable receptor/channel complex. Studies suggest that a loss of function of the complex below an indeterminate threshold triggers cyst initiation, which ultimately results in dysregulation of multiple metabolic processes and downstream pathways and subsequent cyst growth. Noncell autonomous factors may also promote cyst growth. In this report, we focus primarily on the process of early cyst formation and factors that contribute to its variability with brief consideration of how new studies suggest this process may be reversible.
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Registered trials
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