Evidence map›Paper›PMID 21441931›Full record

ArticleNature genetics2011

Common variation in GPC5 is associated with acquired nephrotic syndrome.

Koji Okamoto, Katsushi Tokunaga, Kent Doi, Toshiro Fujita, Hodaka Suzuki, Tetsuo Katoh, Tsuyoshi Watanabe, Nao Nishida, Akihiko Mabuchi, Atsushi Takahashi and 4 more

Abstract read
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In one paragraph

Article in Nature genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Article
  3. Multi-organ imaging-derived polygenic indexes for brain and body health.medRxiv : the preprint server for health sciences · 2024
    Article
  4. Role of non-coding variants in cardiovascular disease.Journal of cellular and molecular medicine · 2023
    Review
  5. Article
  6. Review
  7. Coreceptor functions of cell surface heparan sulfate proteoglycans.American journal of physiology. Cell physiology · 2022
    Review
  8. The function of glypicans in the mammalian embryo.American journal of physiology. Cell physiology · 2022
    Review
  9. Article
  10. Article
  11. Trends in pediatric nephrotic syndrome.World journal of nephrology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Genetic Disorders of the Glomerular Filtration Barrier.Clinical journal of the American Society of Nephrology : CJASN · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Treatment of steroid-resistant nephrotic syndrome in the genomic era.Pediatric nephrology (Berlin, Germany) · 2019
    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

14 authors at 4 institutions in 1 country.

Koji OkamotoDepartment of Nephrology and Endocrinology, University Hospital, The University of Tokyo, Tokyo, Japan.
Katsushi Tokunaga
Kent Doi
Toshiro Fujita
Hodaka Suzuki
Tetsuo Katoh
Tsuyoshi Watanabe
Nao Nishida
Akihiko Mabuchi
Atsushi Takahashi
Michiaki Kubo
Shiro Maeda
Yusuke Nakamura
Eisei Noiri
The University of Tokyo · JPUniversity of Tokyo Hospital · JPFukushima Medical University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe proteinuria is a defining factor of nephrotic syndrome irrespective of the etiology. Investigation of congenital nephrotic syndrome has shown that dysfunction of glomerular epithelial cells (podocytes) plays a crucial role in this disease. Acquired nephrotic syndrome is also assumed to be associated with podocyte injury. Here we identify an association between variants in GPC5, encoding glypican-5, and acquired nephrotic syndrome through a genome-wide association study and replication analysis (P value under a recessive model (P(rec)) = 6.0 × 10(-11), odds ratio = 2.54). We show that GPC5 is expressed in podocytes and that the risk genotype is associated with higher expression. We further show that podocyte-specific knockdown and systemic short interfering RNA injection confers resistance to podocyte injury in mouse models of nephrosis. This study identifies GPC5 as a new susceptibility gene for nephrotic syndrome and implicates GPC5 as a promising therapeutic target for reducing podocyte vulnerability in glomerular disease.

Indexed as

AdultAgedAnimalsBase SequenceCase-Control StudiesDisease Models, AnimalDNA PrimersFemaleGene Knockdown TechniquesGenome-Wide Association StudyGlypicansHumansMaleMiceMiddle AgedModels, GeneticDNA PrimersGlypicansGPC5 protein, humanGpc5 protein, mouseRNA, MessengerRNA, Small Interfering

Identifiers

PMID21441931
OpenAlexW2090364967

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.