Evidence map›Paper›PMID 40199893›Full record

ArticleNature communications2025

The integrin repertoire drives YAP-dependent epithelial:stromal interactions during injury of the kidney glomerulus.

Evelyne Huynh-Cong, Victoria Driscoll, Sandrine Ettou, Keith Keller, Amha Atakilit, Mary E Taglienti, Saurabh Kumar, Astrid Weins, Valerie A Schumacher, Jordan A Kreidberg

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

10 authors.

Evelyne Huynh-CongDepartment of Urology, Boston Children's Hospital, Boston, MA, USA.
Victoria DriscollDivision of Nephrology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Sandrine EttouDepartment of Urology, Boston Children's Hospital, Boston, MA, USA.
Keith KellerDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Amha AtakilitLung Biology Center, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
Mary E TaglientiDepartment of Urology, Boston Children's Hospital, Boston, MA, USA.
Saurabh KumarDepartment of Urology, Boston Children's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0001-8655-9187
Astrid WeinsDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Valerie A SchumacherDepartment of Urology, Boston Children's Hospital, Boston, MA, USA. VSchumac@bidmc.harvard.edu.ORCID http://orcid.org/0000-0001-8670-0486
Jordan A KreidbergDepartment of Urology, Boston Children's Hospital, Boston, MA, USA. Jkreidbe@bidmc.harvard.edu.ORCID http://orcid.org/0000-0002-9085-2420

Funding

U.S. Department of Defense (United States Department of Defense) PR211099
6 · The paper itself

Abstract

The kidney glomerulus is a filtration barrier in which capillary loop architecture depends on epithelial-stromal interactions between podocytes and mesangial cells. Podocytes are terminally differentiated cells within the glomerulus that express YAP and TAZ. Here we test the hypotheses that YAP and TAZ are required in podocytes to maintain capillary loop architecture and that shifts in the integrin repertoire during podocyte injury affect transcriptional activity of YAP and TAZ. Loss of YAP in podocytes of adult mice renders them more sensitive to injury, whereas loss of both YAP and TAZ in podocytes rapidly compromises the filtration barrier. α3β1 and αvβ5 are two prominent integrins on murine podocytes. Podocyte injury or loss of α3β1 leads to increased abundance of αvβ5 and nuclear localization of YAP. In vitro, blockade of αvβ5 decreases nuclear YAP. Increased αv integrins are found in human kidney disease. Thus, our studies demonstrate the crucial regulatory interplay between cell adhesion and transcriptional regulation as an important determinant of human disease.

Indexed as

Adaptor Proteins, Signal TransducingIntegrin alpha3beta1IntegrinsKidney GlomerulusPhosphoproteinsPodocytesReceptors, VitronectinAnimalsCell AdhesionCell Cycle ProteinsEpithelial CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutAdaptor Proteins, Signal TransducingCell Cycle ProteinsIntegrin alpha3beta1IntegrinsPhosphoproteinsReceptors, VitronectinTrans-ActivatorsTranscription FactorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID40199893
PMCPMC11978898

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.