Evidence map›Paper›PMID 32325185›Full record

ReviewCellular signalling2020

STAT signaling in polycystic kidney disease.

Sebastian Strubl, Jacob A Torres, Alison K Spindt, Hannah Pellegrini, Max C Liebau, Thomas Weimbs

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Polycystin-1 Controls Cell Cycle Kinetics, Cell Cycle Exit, and Differentiation of Neural Progenitor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Article
  6. The mutual interaction of TRPC5 channel with polycystin proteins.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
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

6 authors at 2 institutions in 2 countries.

Sebastian StrublDepartment of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA; Department II of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Jacob A TorresDepartment of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA.
Alison K SpindtDepartment of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA.
Hannah PellegriniDepartment of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA.
Max C LiebauDepartment of Pediatrics and Center for Molecular Medicine Cologne, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany; Department II of Internal Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Thomas WeimbsDepartment of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, CA 93106-9625, USA. Electronic address: weimbs@ucsb.edu.
University of California, Santa Barbara · USUniversity of Cologne · DE

Funding

Role of renal crystal deposition in the progression of polycystic kidney diseaseR01DK109563 · NIDDK · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI WEIMBS, THOMAS · 2017 to 2020
$1.4M
NIDDK NIH HHS R01 DK109563
6 · The paper itself

Abstract

The most common form of polycystic kidney disease (PKD) in humans is caused by mutations in the PKD1 gene coding for polycystin1 (PC1). Among the many identified or proposed functions of PC1 is its ability to regulate the activity of transcription factors of the STAT family. Most STAT proteins that have been investigated were found to be aberrantly activated in kidneys in PKD, and some have been shown to be drivers of disease progression. In this review, we focus on the role of signal transducer and activator of transcription (STAT) signaling pathways in various renal cell types in healthy kidneys as compared to polycystic kidneys, on the mechanisms of STAT regulation by PC1 and other factors, and on the possibility to target STAT signaling for PKD therapy.

Indexed as

Signal TransductionAnimalsHumansJanus KinasesKidneyModels, BiologicalPolycystic Kidney DiseasesSTAT Transcription FactorsJanus KinasesSTAT Transcription Factors

Identifiers

PMID32325185
PMCPMC7269822
OpenAlexW3018116912

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.