Evidence map›Paper›PMID 25145933›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Inactivation of integrin-β1 prevents the development of polycystic kidney disease after the loss of polycystin-1.

Kyung Lee, Sylvia Boctor, Laura M C Barisoni, G Luca Gusella

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. TargetingbioRxiv : the preprint server for biology · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Notch2 Inhibition and Kidney Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  14. Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Leucine-Rich Repeat in Polycystin-1 Suppresses Cystogenesis in a Zebrafish (International journal of molecular sciences · 2024
    Article
  19. Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023
    Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Kyung LeeDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and kim.lee@mssm.edu luca.gusella@mssm.edu.
Sylvia BoctorDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and.
Laura M C BarisoniDepartment of Pathology, University of Miami, Miami, Florida.
G Luca GusellaDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and kim.lee@mssm.edu luca.gusella@mssm.edu.
Icahn School of Medicine at Mount Sinai · USUniversity of Miami · US

Funding

Role of polycystin-1 in centrosome duplication and cell cycle controlR01DK078231 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GUSELLA, GABRIELE LUCA · 2008 to 2010
$862k
NIDDK NIH HHS 5R01-DK78231NIDDK NIH HHS R01 DK078231
6 · The paper itself

Abstract

Dysregulation of polycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a disorder characterized by the formation of multiple bilateral renal cysts, the progressive accumulation of extracellular matrix (ECM), and the development of tubulointerstitial fibrosis. Correspondingly, cystic epithelia express higher levels of integrins (ECM receptors that control various cellular responses, such as cell proliferation, migration, and survival) that are characteristically altered in cystic cells. To determine whether the altered expression of ECM and integrins could establish a pathologic autostimulatory loop, we tested the role of integrin-β1 in vitro and on the cystic development of ADPKD in vivo. Compared with wild-type cells, PC1-depleted immortalized renal collecting duct cells had higher levels of integrin-β1 and fibronectin and displayed increased integrin-mediated signaling in the presence of Mn(2+). In mice, conditional inactivation of integrin-β1 in collecting ducts resulted in a dramatic inhibition of Pkd1-dependent cystogenesis with a concomitant suppression of fibrosis and preservation of normal renal function. Our data provide genetic evidence that a functional integrin-β1 is required for the early events leading to renal cystogenesis in ADPKD and suggest that the integrin signaling pathway may be an effective therapeutic target for slowing disease progression.

Indexed as

AnimalsCell LineFibrosisIntegrin beta1KidneyMicePolycystic Kidney DiseasesTRPP Cation ChannelsIntegrin beta1TRPP Cation Channelsautosomal dominant polycystic kidney diseasecell–matrix interactionsfibrosisgenetic renal diseasepolycystic kidney disease

Identifiers

PMID25145933
PMCPMC4378096
OpenAlexW2169316465

What OpenQuestion holds

Textmetadata
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.