Evidence map›Paper›PMID 20219615›Full record

ReviewAdvances in chronic kidney disease2010

Molecular advances in autosomal dominant polycystic kidney disease.

Anna Rachel Gallagher, Gregory G Germino, Stefan Somlo

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
9.5field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Glycosylation in kidney diseases.Precision clinical medicine · 2025
    Review
  5. Adamts1 and Cyst Expansion in Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  6. Article
  7. Autosomal Dominant Polycystic Kidney Disease: Extrarenal Involvement.International journal of molecular sciences · 2024
    Review
  8. Cardiovascular Manifestations and Management in ADPKD.Kidney international reports · 2023
    Review
  9. Review
  10. Review
  11. Ameliorating liver disease in an autosomal recessive polycystic kidney disease mouse model.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  12. Review
  13. Review
  14. RecessiveFrontiers in molecular neuroscience · 2022
    Article
  15. Article
  16. Quinomycin A reduces cyst progression in polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  17. Review
  18. Article
  19. Article
  20. Infectious Disease Risk in Dialysis Patients: A Transdisciplinary Approach.Canadian journal of kidney health and disease · 2019
    Review

27 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Anna Rachel GallagherDepartments of Internal Medicine and Genetics, Yale School of Medicine, New Haven, CT 06520-8029, USA.
Gregory G Germino
Stefan Somlo
National Institutes of Health · US

Funding

The role of PKD proteins in regulating tubular morphologyZIADK075042 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GERMINO, GREGORY · 2010 to 2025
$23.3M
YALE CENTER FOR THE STUDY OF POLYCYSTIC KIDNEY DISEASEP50DK057328 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 1999 to 2009
$11.1M
GENETICS OF AUTOSOMAL DOMINANT POLYCYSTIC LIVER DISEASER01DK051041 · NIDDK · YESHIVA UNIVERSITY · PI SOMLO, STEFAN · 1995 to 2010
$3.4M
MOUSE MODELS OF POLYCYSTIC KIDNEY DISEASE (PKD2)R01DK054053 · NIDDK · YESHIVA UNIVERSITY · PI SOMLO, STEFAN · 1998 to 2015
$3.2M
Intramural NIH HHS Z99 DK999999NIDDK NIH HHS DK51041NIDDK NIH HHS DK54053NIDDK NIH HHS DK57328NIDDK NIH HHS P50 DK057328NIDDK NIH HHS R01 DK051041NIDDK NIH HHS R01 DK054053
6 · The paper itself

Abstract

Autosomal dominant polycystic disease (ADPKD) is the most common form of inherited kidney disease that results in renal failure. The understanding of the pathogenesis of ADPKD has advanced significantly since the discovery of the 2 causative genes, PKD1 and PKD2. Dominantly inherited gene mutations followed by somatic second-hit mutations inactivating the normal copy of the respective gene result in renal tubular cyst formation that deforms the kidney and eventually impairs its function. The respective gene products, polycystin-1 and polycystin-2, work together in a common cellular pathway. Polycystin-1, a large receptor molecule, forms a receptor-channel complex with polycystin-2, which is a cation channel belonging to the TRP family. Both polycystin proteins have been localized to the primary cilium, a nonmotile microtubule-based structure that extends from the apical membrane of tubular cells into the lumen. Here we discuss recent insights in the pathogenesis of ADPKD including the genetics of ADPKD, the properties of the respective polycystin proteins, the role of cilia, and some cell-signaling pathways that have been implicated in the pathways related to PKD1 and PKD2.

Indexed as

Polycystic Kidney, Autosomal DominantAnimalsCiliaHumansProtein Structure, TertiarySignal TransductionTRPP Cation ChannelsTRPP Cation Channels

Identifiers

PMID20219615
PMCPMC2837604
OpenAlexW2114129426

What OpenQuestion holds

Textmetadata
LicenceTDM
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.