Evidence map›Paper›PMID 17975706›Full record

ReviewCellular and molecular life sciences : CMLS2008

Polycystic kidney diseases: from molecular discoveries to targeted therapeutic strategies.

O Ibraghimov-Beskrovnaya, N Bukanov

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  12. Review
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  15. Article
  16. Analysis of the REJ Module of Polycystin-1 Using Molecular Modeling and Force-Spectroscopy Techniques.Journal of biophysics (Hindawi Publishing Corporation : Online) · 2013
    Article
  17. Article
  18. Review
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

O Ibraghimov-BeskrovnayaCell Biology, Genzyme Corporation, 5 Mountain Road, Framingham, MA 01701-9322, USA. oxana.beskrovnaya@genzyme.com
N Bukanov
SynZyme Technologies (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic kidney diseases (PKDs) represent a large group of progressive renal disorders characterized by the development of renal cysts leading to end-stage renal disease. Enormous strides have been made in understanding the pathogenesis of PKDs and the development of new therapies. Studies of autosomal dominant and recessive polycystic kidney diseases converge on molecular mechanisms of cystogenesis, including ciliary abnormalities and intracellular calcium dysregulation, ultimately leading to increased proliferation, apoptosis and dedifferentiation. Here we review the pathobiology of PKD, highlighting recent progress in elucidating common molecular pathways of cystogenesis. We discuss available models and challenges for therapeutic discovery as well as summarize the results from preclinical experimental treatments targeting key disease-specific pathways.

Indexed as

Cell AdhesionCell CycleHumansKidney Failure, ChronicModels, MolecularMutationPolycystic Kidney, Autosomal DominantPolycystic Kidney DiseasesProtein ConformationReceptors, Cell SurfaceTRPP Cation ChannelsPKHD1 protein, humanReceptors, Cell SurfaceTRPP Cation Channels

Identifiers

PMID17975706
PMCPMC2775119
OpenAlexW2035339983

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.