Evidence map›Paper›PMID 27649757›Full record

ArticleBMC nephrology2016

Relationship of clusterin with renal inflammation and fibrosis after the recovery phase of ischemia-reperfusion injury.

Jia Guo, Qiunong Guan, Xiuheng Liu, Hao Wang, Martin E Gleave, Christopher Y C Nguan, Caigan Du

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 76 citations in OpenAlex.

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  13. Urinary Concentration of Renal Biomarkers in Healthy Term Neonates: Gender Differences in GST-pi Excretion.Medical science monitor : international medical journal of experimental and clinical research · 2024
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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

7 authors at 3 institutions in 2 countries.

Jia GuoDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada.
Qiunong GuanDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada.
Xiuheng LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Hao WangDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, China.
Martin E GleaveDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada.
Christopher Y C NguanDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada.
Caigan DuDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada. caigan@mail.ubc.ca.
University of British Columbia · CARenmin Hospital of Wuhan University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong-term outcomes after acute kidney injury (AKI) include incremental loss of function and progression towards chronic kidney disease (CKD); however, the pathogenesis of AKI to CKD remains largely unknown. Clusterin (CLU) is a chaperone-like protein that reduces ischemia-reperfusion injury (IRI) and enhances tissue repair after IRI in the kidney. This study investigated the role of CLU in the transition of IRI to renal fibrosis.

methodsIRI was induced in the left kidneys of wild type (WT) C57BL/6J (B6) versus CLU knockout (KO) B6 mice by clamping the renal pedicles for 28 min at the body temperature of 32 °C. Tissue damage was examined by histology, infiltrate phenotypes by flow cytometry analysis, and fibrosis-related gene expression by PCR array.

resultsReduction of kidney weight was induced by IRI, but was not affected by CLU KO. Both WT and KO kidneys had similar function with minimal cellular infiltration and fibrosis at day 14 of reperfusion. After 30 days, KO kidneys had greater loss in function than WT, indicated by the higher levels of both serum creatinine and BUN in KO mice, and exhibited more cellular infiltration (CD8 cells and macrophages), more tubular damage and more severe tissue fibrosis (glomerulopathy, interstitial fibrosis and vascular fibrosis). PCR array showed the association of CLU deficiency with up-regulation of CCL12, Col3a1, MMP9 and TIMP1 and down-regulation of EGF in these kidneys.

conclusionOur data suggest that CLU deficiency worsens renal inflammation and tissue fibrosis after IRI in the kidney, which may be mediated through multiple pathways.

Indexed as

AnimalsBiomarkersClusterinFibrosisMaleMiceMice, Inbred C57BLMice, KnockoutNephritisRecovery of FunctionReperfusion InjuryBiomarkersClu protein, mouseClusterinAcute kidney injuryChronic kidney diseaseClusterinFibrosisKidney ischemia-reperfusion

Identifiers

PMID27649757
PMCPMC5028988
OpenAlexW2521606514

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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.