ReviewNature reviews. Nephrology2014
Translational research in ADPKD: lessons from animal models.
Review in Nature reviews. Nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 97 citations in OpenAlex.
- Genetic kidney diseases: Decoding molecular taxonomies to drive precision nephrology and therapeutic innovation.Genes & diseases · 2027Review
- GV-001, An Oral Available Histone Deacetylase 6 Inhibitor for the Treatment of Autosomal Dominant Polycystic Kidney Disease.Journal of medicinal chemistry · 2026Article
- Molecular pathology and cystogenic propensity of the ADPKD Taiwan founder variant.JCI insight · 2025Article
- PKD1 mutation perturbs morphogenesis in tubular epithelial organoids derived from human pluripotent stem cells.Scientific reports · 2025Article
- The pathophysiological significance between autosomal dominant polycystic kidney disease and neutrophil gelatinase-associated lipocalin.Kidney research and clinical practice · 2025Article
- Targeting TRPM3 as a potential therapeutic approach for autosomal dominant polycystic kidney disease.Scientific reports · 2025Article
- Genome-Based Advances in Modeling Renal Ciliopathies and Enhancing Patient Care.Kidney & blood pressure research · 2025Review
- Review
- Severity of polycystic kidney disease revealed by multiparametric MRI.Magnetic resonance in medicine · 2023Article
- Polycystin Channel Complexes.Annual review of physiology · 2023Review
- SCF-SKP2 E3 ubiquitin ligase links mTORC1/ER stress/ISR with YAP activation in murine renal cystogenesis.The Journal of clinical investigation · 2022Article
- Effects of Suramin on Polycystic Kidney Disease in a Mouse Model of Polycystin-1 Deficiency.International journal of molecular sciences · 2022Article
- Review
- Generation of heterozygous PKD1 mutant pigs exhibiting early-onset renal cyst formation.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Quantitative Proteomic Study Unmasks Fibrinogen Pathway in Polycystic Liver Disease.Biomedicines · 2022Article
- Establishment of transgenic pigs overexpressing humanFrontiers in genetics · 2022Article
- Studying Kidney Diseases Using Organoid Models.Frontiers in cell and developmental biology · 2022Review
- Reversing polycystic kidney disease.Nature genetics · 2021Article
- Disrupting polycystin-2 EF hand CaJournal of cell science · 2020Article
- Association of autosomal dominant polycystic kidney disease, asymptomatic multiple giant coronary arteries aneurysms and abdominal aortic aneurysm: a case report.Oxford medical case reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or PKD2, which encode polycystin-1 and polycystin-2, respectively. Rodent models are available to study the pathogenesis of polycystic kidney disease (PKD) and for preclinical testing of potential therapies-either genetically engineered models carrying mutations in Pkd1 or Pkd2 or models of renal cystic disease that do not have mutations in these genes. The models are characterized by age at onset of disease, rate of disease progression, the affected nephron segment, the number of affected nephrons, synchronized or unsynchronized cyst formation and the extent of fibrosis and inflammation. Mouse models have provided valuable mechanistic insights into the pathogenesis of PKD; for example, mutated Pkd1 or Pkd2 cause renal cysts but additional factors are also required, and the rate of cyst formation is increased in the presence of renal injury. Animal studies have also revealed complex genetic and functional interactions among various genes and proteins associated with PKD. Here, we provide an update on the preclinical models commonly used to study the molecular pathogenesis of ADPKD and test potential therapeutic strategies. Progress made in understanding the pathophysiology of human ADPKD through these animal models is also discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.