ArticleThe American journal of pathology2010
Hepato-renal pathology in pkd2ws25/- mice, an animal model of autosomal dominant polycystic kidney disease.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools.Physiological reviews · 2026Review
- Can micro-CT distinguish between solid lung tumors? A comparative evaluation including solid adenocarcinoma, non-keratinizing squamous cell carcinoma, and carcinoid tumor.Journal of pathology and translational medicine · 2026Article
- Pathogenic Pathways and Therapeutic Strategies in Autosomal Dominant Polycystic Kidney Disease (ADPKD).Journal of cellular signaling · 2025Article
- Review
- Genetics, pathobiology and therapeutic opportunities of polycystic liver disease.Nature reviews. Gastroenterology & hepatology · 2022Review
- Polycystic Liver Disease: Advances in Understanding and Treatment.Annual review of pathology · 2022Review
- Renal plasticity revealed through reversal of polycystic kidney disease in mice.Nature genetics · 2021Article
- Intraflagellar Transport Proteins as Regulators of Primary Cilia Length.Frontiers in cell and developmental biology · 2021Review
- A mild reduction of food intake slows disease progression in an orthologous mouse model of polycystic kidney disease.American journal of physiology. Renal physiology · 2016Article
- Polycystic liver diseases: advanced insights into the molecular mechanisms.Nature reviews. Gastroenterology & hepatology · 2014Review
- Centrosomal abnormalities characterize human and rodent cystic cholangiocytes and are associated with Cdc25A overexpression.The American journal of pathology · 2014Article
- The zebrafish as a model to study polycystic liver disease.Zebrafish · 2013Article
- Polycystic kidneys have decreased vascular density: a micro-CT study.Microcirculation (New York, N.Y. : 1994) · 2013Article
- Review
- Endothelial dysfunction occurs prior to clinical evidence of polycystic kidney disease.American journal of nephrology · 2013Article
- Functional polycystin-1 dosage governs autosomal dominant polycystic kidney disease severity.The Journal of clinical investigation · 2012Article
- The extracellular matrix and ciliary signaling.Current opinion in cell biology · 2012Review
- Inhibition of Cdc25A suppresses hepato-renal cystogenesis in rodent models of polycystic kidney and liver disease.Gastroenterology · 2012Article
- The primary cilium in different tissues-lessons from patients and animal models.Pediatric nephrology (Berlin, Germany) · 2011Review
- Biliary exosomes influence cholangiocyte regulatory mechanisms and proliferation through interaction with primary cilia.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystic liver diseases, the most important of which are autosomal dominant and autosomal recessive polycystic kidney diseases, are incurable pathological conditions. Animal models that resemble human pathology in these diseases provide an opportunity to study the mechanisms of cystogenesis and to test potential treatments. Here we demonstrate that Pkd2ws25/- mice, an animal model of autosomal dominant polycystic kidney disease, developed hepatic cysts. As assessed by micro-computed tomography scanning of intact livers and by light microscopy of hepatic tissue, hepatic cystic volumes increased from 12.82+/-3.16% (5- to 8-month-old mice) to 21.58+/-4.81% (9- to 12-month-old mice). Renal cystogenesis was more severe at early stages of disease: in 5- to 7-month-old mice, cystic volumes represented 40.67+/-5.48% of kidney parenchyma, whereas in older mice cysts occupied 31.04+/-1.88% of kidney parenchyma. Mild fibrosis occurred only in liver, and its degree was unchanged with age. Hepatic cysts were lined by single or multiple layers of squamous cholangiocytes. Cystic cholangiocyte cilia were short and malformed, whereas in renal cysts they appeared normal. In Pkd2ws25/- mice, mitotic and apoptotic indices in both kidney and liver were increased compared with wild-type mice. In conclusion, Pkd2ws25/- mice exhibit hepatorenal pathology resembling human autosomal dominant polycystic kidney disease and represent a useful model to study mechanisms of cystogenesis and to evaluate treatment options.
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.