Evidence map›Paper›PMID 25629817›Full record

ArticlePloS one2015

Knockout of the TauT gene predisposes C57BL/6 mice to streptozotocin-induced diabetic nephropathy.

Xiaobin Han, Andrea B Patters, Takashi Ito, Junichi Azuma, Stephen W Schaffer, Russell W Chesney

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 2 institutions in 2 countries.

Xiaobin HanDepartment of Pediatrics, University of Tennessee Health Science Center, and the Children's Foundation Research Institute at Le Bonheur Children's Hospital, Memphis, TN, United States of America.
Andrea B PattersDepartment of Pediatrics, University of Tennessee Health Science Center, and the Children's Foundation Research Institute at Le Bonheur Children's Hospital, Memphis, TN, United States of America.
Takashi ItoDepartment of Pharmacy, College of Pharmacy, Hyogo University, Kobe, Japan.
Junichi AzumaDepartment of Pharmacy, College of Pharmacy, Hyogo University, Kobe, Japan.
Stephen W SchafferDepartment of Pharmacology, University of South Alabama, Mobile, AL, United States of America.
Russell W ChesneyDepartment of Pediatrics, University of Tennessee Health Science Center, and the Children's Foundation Research Institute at Le Bonheur Children's Hospital, Memphis, TN, United States of America.
Hyogo University · JPUniversity of South Alabama · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is the leading cause of end stage renal disease in the world. Although tremendous efforts have been made, scientists have yet to identify an ideal animal model that can reproduce the characteristics of human diabetic nephropathy. In this study, we hypothesize that taurine insufficiency is a critical risk factor for development of diabetic nephropathy associated with diabetes mellitus. This hypothesis was tested in vivo in TauT heterozygous (TauT+/-) and homozygous (TauT-/-) knockout in C57BL/6 background mice. We have shown that alteration of the TauT gene (also known as SLC6A6) has a substantial effect on the susceptibility to development of extensive diabetic kidney disease in both TauT+/- and TauT-/-mouse models of diabetes. These animals developed histological changes characteristic of human diabetic nephropathy that included glomerulosclerosis, nodular lesions, arteriosclerosis, arteriolar dilation, and tubulointerstitial fibrosis. Immunohistochemical staining of molecular markers of smooth muscle actin, CD34, Ki67 and collagen IV further confirmed these observations. Our results demonstrated that both homozygous and heterozygous TauT gene deletion predispose C57BL/6 mice to develop end-stage diabetic kidney disease, which closely replicates the pathological features of diabetic nephropathy in human diabetic patients.

Indexed as

ActinsAnimalsCollagen Type IVDiabetes Mellitus, ExperimentalDiabetic RetinopathyGenetic Predisposition to DiseaseMembrane GlycoproteinsMembrane Transport ProteinsMiceMice, Inbred C57BLMice, KnockoutTaurine TransportersActinsCollagen Type IVMembrane GlycoproteinsMembrane Transport ProteinsTaurine Transporters

Identifiers

PMID25629817
PMCPMC4309680
OpenAlexW2081279079

What OpenQuestion holds

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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.