ArticlePLoS genetics2012
Network analysis of a Pkd1-mouse model of autosomal dominant polycystic kidney disease identifies HNF4α as a disease modifier.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 93 citations in OpenAlex.
- Urinary metabolites associate with the rate of kidney function decline in patients with autosomal dominant polycystic kidney disease.PloS one · 2020Trial
- Plasma metabolites and lipids associate with kidney function and kidney volume in hypertensive ADPKD patients early in the disease course.BMC nephrology · 2019Trial
- Kidney-specific deletion of the BicC family RNA-binding protein 1 triggers an ADPKD-like cystogenic program.iScience · 2026Article
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Kidney Volume and Molecular Processes are Dynamic in ADPKD.Kidney international reports · 2026Article
- Vascular transcriptional and metabolic changes precede progressive intrarenal microvascular rarefaction in autosomal dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2026Article
- Inactivation of Pkd2 in adult mice results in delayed cyst formation and identifies sex as a major modifier of disease severity.Kidney international · 2026Article
- Abnormal purinergic signaling contributes to development of renal cysts in autosomal dominant polycystic kidney disease.Purinergic signalling · 2026Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- A Computational Protocol for the Knowledge-Based Assessment and Capture of Pathologies.Methods in molecular biology (Clifton, N.J.) · 2025Article
- A brief harvesting-freezing delay significantly alters the kidney metabolome and leads to false positive and negative results.American journal of physiology. Renal physiology · 2024Article
- Review
- Potential Add-On Benefits of Dietary Intervention in the Treatment of Autosomal Dominant Polycystic Kidney Disease.Nutrients · 2024Review
- Reprogramming of Energy Metabolism in HumanInternational journal of molecular sciences · 2024Article
- Deletion of Aurora kinase A prevents the development of polycystic kidney disease in mice.Nature communications · 2024Article
- Editorial: Hepatocyte nuclear factor 4 alpha - new insights into an old receptor.Frontiers in endocrinology · 2024Article
- Short salsalate administration affects cell proliferation, metabolism, and inflammation in polycystic kidney disease.iScience · 2023Article
- Mechanisms of Cyst Development in Polycystic Kidney Disease.Advances in kidney disease and health · 2023Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Autosomal Dominant Polycystic Kidney Disease (ADPKD; MIM ID's 173900, 601313, 613095) leads to end-stage kidney disease, caused by mutations in PKD1 or PKD2. Inactivation of Pkd1 before or after P13 in mice results in distinct early- or late-onset disease. Using a mouse model of ADPKD carrying floxed Pkd1 alleles and an inducible Cre recombinase, we intensively analyzed the relationship between renal maturation and cyst formation by applying transcriptomics and metabolomics to follow disease progression in a large number of animals induced before P10. Weighted gene co-expression network analysis suggests that Pkd1-cystogenesis does not cause developmental arrest and occurs in the context of gene networks similar to those that regulate/maintain normal kidney morphology/function. Knowledge-based Ingenuity Pathway Analysis (IPA) software identifies HNF4α as a likely network node. These results are further supported by a meta-analysis of 1,114 published gene expression arrays in Pkd1 wild-type tissues. These analyses also predict that metabolic pathways are key elements in postnatal kidney maturation and early steps of cyst formation. Consistent with these findings, urinary metabolomic studies show that Pkd1 cystic mutants have a distinct profile of excreted metabolites, with pathway analysis suggesting altered activity in several metabolic pathways. To evaluate their role in disease, metabolic networks were perturbed by inactivating Hnf4α and Pkd1. The Pkd1/Hnf4α double mutants have significantly more cystic kidneys, thus indicating that metabolic pathways could play a role in Pkd1-cystogenesis.
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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.