Evidence map›Paper›PMID 24586548›Full record

ArticlePloS one2014

Twisted gastrulation, a BMP antagonist, exacerbates podocyte injury.

Sachiko Yamada, Jin Nakamura, Misako Asada, Masayuki Takase, Taiji Matsusaka, Taku Iguchi, Ryo Yamada, Mari Tanaka, Atsuko Y Higashi, Tomohiko Okuda and 10 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Multifaceted Functions of TWSG1: From Embryogenesis to Cancer Development.International journal of molecular sciences · 2022
    Review
  3. Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Agonists and Antagonists of TGF-β Family Ligands.Cold Spring Harbor perspectives in biology · 2016
    Review
  6. Review
  7. Role of Smad signaling in kidney disease.International urology and nephrology · 2015
    Review
  8. Article
  9. 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

20 authors at 9 institutions in 3 countries.

Sachiko YamadaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Jin NakamuraDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Misako AsadaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Masayuki TakaseDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Taiji MatsusakaDepartment of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Taku IguchiTMK Project, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan.
Ryo YamadaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Mari TanakaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Atsuko Y HigashiDeaprtment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Tomohiko OkudaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Nariaki AsadaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Atsushi FukatsuYachiyo Hospital, Anjyo, Aichi, Japan.
Hiroshi KawachiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Niigata, Japan.
Daniel GrafInstitute of Oral Biology, Faculty of Medicine, University of Zurich, Zurich, Switzerland.
Eri MusoDepartment of Nephrology and Dialysis, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Osaka, Japan.
Toru KitaKobe City Medical Center General Hospital, Kobe, Hyogo, Japan.
Takeshi KimuraDeaprtment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Ira PastanLaboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Aris N EconomidesRegeneron Pharmaceuticals, Inc., Tarrytown, New York, United States of America.
Motoko YanagitaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Kyoto, Japan.
Kyoto University · JPKitano Hospital · JPKobe City Medical Center General Hospital · JPNational Cancer Institute · USNational Sanyo Hospital · JPNiigata University · JPRegeneron (United States) · USTokai University · JPUniversity of Zurich · CH

Funding

Immunotoxin Therapy of Solid and Hematopoietic Tumors: Preclinical StudiesZIABC008753 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PASTAN, IRA · 2009 to 2024
$33.1M
6 · The paper itself

Abstract

Podocyte injury is the first step in the progression of glomerulosclerosis. Previous studies have demonstrated the beneficial effect of bone morphogenetic protein 7 (Bmp7) in podocyte injury and the existence of native Bmp signaling in podocytes. Local activity of Bmp7 is controlled by cell-type specific Bmp antagonists, which inhibit the binding of Bmp7 to its receptors. Here we show that the product of Twisted gastrulation (Twsg1), a Bmp antagonist, is the central negative regulator of Bmp function in podocytes and that Twsg1 null mice are resistant to podocyte injury. Twsg1 was the most abundant Bmp antagonist in murine cultured podocytes. The administration of Bmp induced podocyte differentiation through Smad signaling, whereas the simultaneous administration of Twsg1 antagonized the effect. The administration of Bmp also inhibited podocyte proliferation, whereas simultaneous administration of Twsg1 antagonized the effect. Twsg1 was expressed in the glomerular parietal cells (PECs) and distal nephron of the healthy kidney, and additionally in damaged glomerular cells in a murine model of podocyte injury. Twsg1 null mice exhibited milder hypoalbuminemia and hyperlipidemia, and milder histological changes while maintaining the expression of podocyte markers during podocyte injury model. Taken together, our results show that Twsg1 plays a critical role in the modulation of protective action of Bmp7 on podocytes, and that inhibition of Twsg1 is a promising means of development of novel treatment for podocyte injury.

Indexed as

AnimalsBone Morphogenetic Protein 7Cell DifferentiationCells, CulturedKidney GlomerulusMiceMice, Inbred C57BLMice, KnockoutNephronsPodocytesProteinsSignal TransductionSmad Proteinsbmp7 protein, mouseBone Morphogenetic Protein 7ProteinsSmad Proteinstwisted gastrulation protein, mouse

Identifiers

PMID24586548
PMCPMC3934867
OpenAlexW2148089677

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.