ReviewJournal of the American Society of Nephrology : JASN2016
Variable Cyst Development in Autosomal Dominant Polycystic Kidney Disease: The Biologic Context.
Review in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- A new conceptual framework for PKD1 in ADPKD; integrating DNA structures and inflammation.BMC nephrology · 2026Review
- Inhibition of the inflammasome ameliorates orthologous polycystic kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hypertension increases PPV for polycystic kidney disease in PKD1 and PKD2 variant carriers.HGG advances · 2025Article
- Kidney organoid models of polycystic kidney disease: challenges and future directions.American journal of physiology. Renal physiology · 2025Review
- Ciliary G-Protein Coupled Receptor Signaling in Polycystic Kidney Disease.International journal of molecular sciences · 2025Review
- Somatic mutation in autosomal dominant polycystic kidney disease revealed by deep sequencing human kidney cysts.NPJ genomic medicine · 2024Article
- Adenine base editor corrected ADPKD point mutations in hiPSCs and kidney organoids.Advanced biotechnology · 2024Article
- Inhibition of pannexin-1 does not restore electrolyte balance in precystic Pkd1 knockout mice.Physiological reports · 2024Article
- Computational drug discovery approaches identify mebendazole as a candidate treatment for autosomal dominant polycystic kidney disease.Frontiers in pharmacology · 2024Article
- Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023Article
- Dehydration Accelerates Cytogenesis and Cyst Growth in Pkd1Inflammation · 2023Article
- Wall Tension and Tubular Resistance in Kidney Cystic Conditions.Biomedicines · 2023Review
- ModelingMolecular therapy. Methods & clinical development · 2023Article
- Mechanism of cystogenesis by Cd79a-driven, conditional mTOR activation in developing mouse nephrons.Scientific reports · 2023Article
- Identification and functional interpretation of miRNAs affected by rare CNVs in CAKUT.Scientific reports · 2022Article
- Loss of function of renal Glut2 reverses hyperglycaemia and normalises body weight in mouse models of diabetes and obesity.Diabetologia · 2022Article
- Review
- Renal plasticity revealed through reversal of polycystic kidney disease in mice.Nature genetics · 2021Article
- Characterization of Primary Cilia in Osteoblasts Isolated From Patients With ADPKD and CKD.JBMR plus · 2021Article
- A Multitubular Kidney-on-Chip to Decipher Pathophysiological Mechanisms in Renal Cystic Diseases.Frontiers in bioengineering and biotechnology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Patients with autosomal dominant polycystic kidney disease (ADPKD) typically carry a mutation in either the PKD1 or PKD2 gene, which leads to massive cyst formation in both kidneys. However, the large intrafamilial variation in the progression rate of ADPKD suggests involvement of additional factors other than the type of mutation. The identification of these factors will increase our understanding of ADPKD and could ultimately help in the development of a clinically relevant therapy. Our review addresses the mechanisms by which various biologic processes influence cyst formation and cyst growth, thereby explaining an important part of the inter- and intrafamilial variability in ADPKD. Numerous studies from many laboratories provide compelling evidence for the influence on cyst formation by spatiotemporal gene inactivation, the genetic context, the metabolic status, the presence of existing cysts, and whether the kidneys were challenged by renal injury. Collectively, a solid basis is provided for the concept that the probability of cyst formation is determined by functional PKD protein levels and the biologic context. We model these findings in a graphic representation called the cystic probability landscape, providing a robust conceptual understanding of why cells sometimes do or do not form cysts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.