Evidence map›Paper›PMID 26846181›Full record

ArticleJournal of biomedical science2016

Significance of the urokinase-type plasminogen activator and its receptor in the progression of focal segmental glomerulosclerosis in clinical and mouse models.

Jin-Shuen Chen, Li-Chien Chang, Chung-Ze Wu, Tzu-Ling Tseng, Jui-An Lin, Yuh-Feng Lin, Chao-Wen Cheng

Erratum issuedOpen access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 10% 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

7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Precision medicine for focal segmental glomerulosclerosis.Kidney research and clinical practice · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Jin-Shuen ChenDivision of Nephrology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, No. 325, Section 2, Chenggong Road, Neihu District, Taipei, 114, Taiwan.
Li-Chien ChangSchool of Pharmacy, National Defense Medical Center, Taipei, Taiwan.
Chung-Ze WuDepartment of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Tzu-Ling TsengBiomedical Technology & Device Research Laboratories, Industrial Technology Research Institute, Hsinchu, Taiwan.
Jui-An LinGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250, Wu-Xing Street, Taipei, 110, Taiwan.
Yuh-Feng LinDepartment of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Chao-Wen ChengGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250, Wu-Xing Street, Taipei, 110, Taiwan. ccheng@tmu.edu.tw.
Taipei Medical University · TWTaipei Medical University-Shuang Ho Hospital · TWIndustrial Technology Research Institute · TWNational Defense Medical Center · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundsuPAR biomarker generally considered a pathogenic factor in FSGS. However, studies have been published that dispute this conclusion. The current study was designed to investigate the roles of uPA and suPAR in FSGS in clinical and mouse models.

methodsClinical subjects including those with biopsy-proven FSGS and MCD were enrolled. To verify the role of uPA in FSGS, Adriamycin was used to induce FSGS in uPA knockout (uPA(-/-)) and BALB/c (WT) mice. Proteinuria and suPAR, the cleaved/intact forms of the circulating suPAR, and possible proteases involving cleavage of the suPAR were also studied.

resultsFSGS clinical cases presented significantly higher serum levels of suPAR and Cr and lower serum levels of uPA. In the mice model, the uPA(-/-) group exhibited faster disease progression and worsening proteinuria than the WT group. In addition, the uPA(-/-) group had higher plasma suPAR levels, glomerular cell apoptosis, and dysregulation of the Th1/Th2 balance. In an analysis of suPAR variants in FSGS, both the intact and cleaved forms of the suPAR were higher in clinical subjects and the mouse model. However, the process of suPAR cleavage was not mediated by enzymatic activities of the uPA, elastase, or cathepsin G.

conclusionsA deficiency of uPA accelerated the progression of Adriamycin-induced mouse FSGS model. Decrease of serum uPA levels may be an indicator of the progression of FSGS in clinical subjects and animal models.

Indexed as

AnimalsDisease Models, AnimalFemaleGlomerulosclerosis, Focal SegmentalHumansKidney GlomerulusMaleMiceMice, Inbred BALB CMice, KnockoutReceptors, Urokinase Plasminogen ActivatorTh1 CellsTh2 CellsUrokinase-Type Plasminogen ActivatorPLAUR protein, humanPlaur protein, mouseReceptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen Activator

Identifiers

PMID26846181
PMCPMC4743092
OpenAlexW2258242478

What OpenQuestion holds

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LicenceCC BY
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.