Evidence map›Paper›PMID 26015453›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Podocyte-Specific Deletion of Yes-Associated Protein Causes FSGS and Progressive Renal Failure.

Monica Schwartzman, Antoine Reginensi, Jenny S Wong, John M Basgen, Kristin Meliambro, Susanne B Nicholas, Vivette D'Agati, Helen McNeill, Kirk N Campbell

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 110 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting the Hippo pathway in cancer.Nature reviews. Drug discovery · 2025
    Review
  9. Review
  10. Article
  11. Balancing YAP and TAZ for Podocyte Survival.Journal of the American Society of Nephrology : JASN · 2025
    Article
  12. Article
  13. Article
  14. CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025
    Article
  15. Article
  16. Nucleoporin-associated steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. The renoprotective effect of Tibolone in sepsis-induced acute kidney injury.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024
    Article

17 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

9 authors at 6 institutions in 2 countries.

Monica SchwartzmanDivision of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York;
Antoine ReginensiLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada;
Jenny S WongDivision of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York;
John M BasgenDepartment of Research, Morphometry and Stereology Laboratory, Charles R. Drew University of Medicine and Science, Los Angeles, California;
Kristin MeliambroDivision of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York;
Susanne B NicholasDepartment of Research, Morphometry and Stereology Laboratory, Charles R. Drew University of Medicine and Science, Los Angeles, California; Department of Medicine, Division of Nephrology, University of California Los Angeles, Los Angeles, California; and.
Vivette D'AgatiDepartment of Pathology, Columbia University College of Physicians and Surgeons, New York, New York.
Helen McNeillLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada;
Kirk N CampbellDivision of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York; kirk.campbell@mssm.edu.
Icahn School of Medicine at Mount Sinai · USCharles R. Drew University of Medicine and Science · USColumbia University · USLunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CAUniversity of California, Los Angeles · US

Funding

Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Jaydutt V. Vadgama · 2012 to 2026
$60.0M
Mount Sinai Nephrology Research Training GrantT32DK007757 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CAMPBELL, KIRK N, HE, JOHN CIJIANG · 1998 to 2022
$3.8M
The role of dendrin in glomerular disease progressionR01DK103022 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CAMPBELL, KIRK N · 2015 to 2019
$1.9M
Regulation of podocyte survival by dendrinK08DK081617 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAMPBELL, KIRK N · 2009 to 2013
$733k
NIDDK NIH HHS DK081617NIDDK NIH HHS K08 DK081617NIDDK NIH HHS R01 DK103022NIDDK NIH HHS T32 DK007757NIMHD NIH HHS U54 MD007598NIMHD NIH HHS U54-MD007598
6 · The paper itself

Abstract

FSGS is the most common primary glomerular disease underlying ESRD in the United States and is increasing in incidence globally. FSGS results from podocyte injury, yet the mechanistic details of disease pathogenesis remain unclear. This has resulted in an unmet clinical need for cell-specific therapy in the treatment of FSGS and other proteinuric kidney diseases. We previously identified Yes-associated protein (YAP) as a prosurvival signaling molecule, the in vitro silencing of which increases podocyte susceptibility to apoptotic stimulus. YAP is a potent oncogene that is a prominent target for chemotherapeutic drug development. In this study, we tested the hypothesis that podocyte-specific deletion of Yap leads to proteinuric kidney disease through increased podocyte apoptosis. Yap was selectively silenced in podocytes using Cre-mediated recombination controlled by the podocin promoter. Yap silencing in podocytes resulted in podocyte apoptosis, podocyte depletion, proteinuria, and an increase in serum creatinine. Histologically, features characteristic of FSGS, including mesangial sclerosis, podocyte foot process effacement, tubular atrophy, interstitial fibrosis, and casts, were observed. In human primary FSGS, we noted reduced glomerular expression of YAP. Taken together, these results suggest a role for YAP as a physiologic antagonist of podocyte apoptosis, the signaling of which is essential for maintaining the integrity of the glomerular filtration barrier. These data suggest potential nephrotoxicity with strategies directed toward inhibition of YAP function. Further studies should evaluate the role of YAP in proteinuric glomerular disease pathogenesis and its potential utility as a therapeutic target.

Indexed as

Gene DeletionAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsDisease ProgressionGlomerulosclerosis, Focal SegmentalHumansMiceMice, KnockoutPhosphoproteinsPodocytesRenal InsufficiencyYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsPhosphoproteinsYap1 protein, mouseYAP-Signaling Proteinsfocal segmental glomerulosclerosisglomerular diseasepodocyte

Identifiers

PMID26015453
PMCPMC4696566
OpenAlexW2103977381

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.