Evidence map›Paper›PMID 23949800›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

Survivin mediates renal proximal tubule recovery from AKI.

Jianchun Chen, Jian-Kang Chen, Edward M Conway, Raymond C Harris

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

67 citing papers in PubMed, 112 citations in OpenAlex.

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  13. The renoprotective effect of Tibolone in sepsis-induced acute kidney injury.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024
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7 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Jianchun ChenDepartment of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Jian-Kang Chen
Edward M Conway
Raymond C Harris
Vanderbilt University · USGeorgia Regents Medical Center · USUniversity of British Columbia · CA

Funding

The Role of the EGF Receptor in Acute and Chronic Renal InjuryR01DK051265 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 1997 to 2026
$10.1M
The role of the innate immune cell cyclooxygenase/prostaglandin system in blood pressureregulationR01DK062794 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2003 to 2026
$9.4M
Mechanism of Compensatory Renal HypertrophyR01DK083575 · NIDDK · VANDERBILT UNIVERSITY · PI CHEN, JIAN-KANG · 2011 to 2015
$1.7M
ADRENAL CORTICAL PHOSPHOPROTEIN PHOSPHATASESF32DK007934 · NIDDK · YALE UNIVERSITY · PI PACHTER, JONATHAN A · 1987 to 1988
–
CIHRNIDDK NIH HHS DK51265NIDDK NIH HHS DK62794NIDDK NIH HHS DK7934NIDDK NIH HHS DK83575NIDDK NIH HHS R01 DK051265NIDDK NIH HHS R01 DK062794NIDDK NIH HHS R01 DK083575
6 · The paper itself

Abstract

AKI induces the renoprotective upregulation of survivin expression in kidney epithelial cells, but the underlying mechanisms have not been identified. To determine the role of survivin in renal recovery from AKI, we generated mice with renal proximal tubule-specific deletion of survivin (survivin(ptKO)). Renal survivin expression increased substantially in response to ischemia-reperfusion (I/R) injury in control littermates but remained minimal in survivin(ptKO) mice. Functional and histologic data indicated similar degrees of renal injury in survivin(ptKO) and control mice 24 hours after reperfusion, but recovery was markedly delayed in survivin(ptKO) mice. In MCT cells, a mouse renal proximal tubule cell line, ATP depletion by antimycin A treatment upregulated survivin expression through a phospho-STAT3-dependent pathway. In wild-type mice, inhibition of STAT3 kinase diminished I/R-induced upregulation of STAT3 phosphorylation and survivin expression and delayed recovery. Furthermore, I/R injury activated Notch-2 signaling, and a γ-secretase inhibitor suppressed I/R-induced Notch-2 signaling, STAT3 phosphorylation, and survivin expression and delayed recovery. In MCT cells, inhibition of γ-secretase similarly attenuated antimycin A-induced Notch-2 activation, upregulation of survivin, and phosphorylation of STAT3, but STAT3 kinase inhibition did not prevent Notch-2 activation. Therefore, these data suggest that STAT3 phosphorylation and subsequent upregulation of survivin expression mediated by Notch-2 signaling in renal proximal tubule epithelial cells aid in the functional and structural recovery of the kidney from AKI.

Indexed as

Acute Kidney InjuryAnimalsAnti-Bacterial AgentsAntimycin ACell LineInhibitor of Apoptosis ProteinsKidney Tubules, ProximalMiceMice, Inbred BALB CMice, KnockoutReceptor, Notch2Recovery of FunctionReperfusion InjuryRepressor ProteinsSTAT3 Transcription FactorSurvivinAnti-Bacterial AgentsAntimycin ABirc5 protein, mouseInhibitor of Apoptosis ProteinsNotch2 protein, mouseReceptor, Notch2Repressor ProteinsStat3 protein, mouseSTAT3 Transcription FactorSurvivin

Identifiers

PMID23949800
PMCPMC3839548
OpenAlexW2150856927

What OpenQuestion holds

Textmetadata
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.