Evidence map›Paper›PMID 29636014›Full record

ArticleBMC genetics2018

Genetic loci for resistance to podocyte injury caused by the tensin2 gene deficiency in mice.

Yuki Takahashi, Hayato Sasaki, Shiori Okawara, Nobuya Sasaki

Open access · diamondAbstract read
In one paragraph

Article in BMC genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Quantitative phenotyping ofAmerican journal of physiology. Renal physiology · 2024
    Article
  4. Article
  5. Review
  6. Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Tensin regulates pharyngeal pumping in Caenorhabditis elegans.Biochemical and biophysical research communications · 2020
    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

4 authors at 1 institution in 1 country.

Yuki TakahashiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, 35-1, Higashi-23, Towada, Aomori, 034-8628, Japan.
Hayato SasakiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, 35-1, Higashi-23, Towada, Aomori, 034-8628, Japan. hsasaki@vmas.kitasato-u.ac.jp.ORCID 0000-0003-0162-4774
Shiori OkawaraLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, 35-1, Higashi-23, Towada, Aomori, 034-8628, Japan.
Nobuya SasakiLaboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, 35-1, Higashi-23, Towada, Aomori, 034-8628, Japan.
Kitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTensin2 is a focal adhesion-localized multidomain protein expressed in various tissues, and its dysfunction leads to alterations in podocytes. However, these podocyte-related manifestations are dependent on murine strain. Tensin2 dysfunction results in susceptible strains developing podocyte foot process effacement and massive albuminuria, whereas podocytes in resistant strains remain almost intact. In our previous studies, quantitative trait loci analysis and congenic analysis using resistant C57BL/6J and susceptible ICGN mice identified a modifier locus associated with podocyte injury caused by tensin2 dysfunction on chromosome 2. However, the effect of this modifier locus on chromosome 2 is insufficient to explain the resistance of C57BL/6J mice to tensin2 dysfunction, indicating the existence of other modifier genes.

resultsWhereas previous studies focused on the severity of chronic kidney disease, the present study focused on podocyte injury. We performed a genome-wide linkage analysis of backcrosses between two tensin2-deficient mouse strains, B6.ICGN-Tns2

conclusionsThese data indicate that the resistance to podocyte injury caused by tensin2 dysfunction is mainly produced by the effects of the modifier genes on the two loci. The identification of these modifier genes is expected to help elucidate the mechanism underlying podocyte injury.

Indexed as

AlbuminuriaAnimalsGenetic LinkageMiceMice, Inbred C57BLPodocytesQuantitative Trait LociRenal Insufficiency, ChronicTensinsTensinsTns2 protein, mouseAlbuminuriaLinkage analysisPodocyteTensin2

Identifiers

PMID29636014
PMCPMC5894168
OpenAlexW2804190831

What OpenQuestion holds

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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.