ReviewJournal of nephropharmacology2016
Pathways, perspectives and pursuits in polycystic kidney disease.
Review in Journal of nephropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects.Molecular medicine (Cambridge, Mass.) · 2020Review
- Centrosome amplification disrupts renal development and causes cystogenesis.The Journal of cell biology · 2018Article
- Insights into cellular and molecular basis for urinary tract infection in autosomal-dominant polycystic kidney disease.American journal of physiology. Renal physiology · 2017Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic kidney disease (PKD) is characterized by the growth of numerous cysts in the kidneys. When cysts form in the kidneys, they are filled with fluid. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure. Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease that occurs in one out of 1000 humans. PKD and its causes are being dissected through studies of human populations and through the use of animal models. Mouse models in particular have made a substantial contribution to our understanding of the gene pathways involved in the pathogenesis and the nature of signaling molecules that act in a tissue-specific manner at critical stages of cyst development. PKD has a number of characteristics that make it uniquely challenging for the development of therapies to slowdown disease progression. This review provides current understanding of the etiopathology, pathways involved and therapeutic targets of PKDs.
Indexed as
Identifiers
28197498PMC5297506W2294324670What 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.