Evidence map›Paper›PMID 26924060›Full record

ReviewKidney international2016

Autophagy in acute kidney injury.

Gur P Kaushal, Sudhir V Shah

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed, 2 pooled it
24.3field-weighted citation impact, top 1% 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

212 citing papers in PubMed, 2 syntheses or guidelines pooled it, 379 citations in OpenAlex.

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152 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

2 authors at 1 institution in 1 country.

Gur P KaushalRenal Section, Medicine Service, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA; Division of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. Electronic address: kaushalgurp@uams.edu.
Sudhir V ShahRenal Section, Medicine Service, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA; Division of Nephrology, Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
University of Arkansas for Medical Sciences · US

Funding

Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
Meprin A Metalloproteinase in Acute Kidney InjuryR01DK081690 · NIDDK · UNIV OF ARKANSAS FOR MED SCIS · PI KAUSHAL, GUR PRASAD · 2010 to 2013
$866k
Role of PPARa on renal fibrosisI01BX000444 · VA · CENTRAL ARKANSAS VETERANS HLTHCARE SYS · PI PORTILLA, DIDIER · 2009 to 2014
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Role of Meprin A in Acute Kidney InjuryI01BX000538 · VA · CENTRAL ARKANSAS VETERANS HLTHCARE SYS · PI KAUSHAL, GUR PRASAD · 2009 to 2013
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Mechanisms of cLDL-Induced Endothelial InjuryI01BX001519 · VA · CENTRAL ARKANSAS VETERANS HLTHCARE SYS · PI SHAH, SUDHIR V · 2012 to 2015
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BLRD VA I01 BX000444BLRD VA I01 BX000538BLRD VA I01 BX001519NCATS NIH HHS UL1 TR000039NCATS NIH HHS UL1TR000039NIDDK NIH HHS R01 DK081690
6 · The paper itself

Abstract

Autophagy is a conserved multistep pathway that degrades and recycles damaged organelles and macromolecules to maintain intracellular homeostasis. The autophagy pathway is upregulated under stress conditions including cell starvation, hypoxia, nutrient and growth-factor deprivation, endoplasmic reticulum stress, and oxidant injury, most of which are involved in the pathogenesis of acute kidney injury (AKI). Recent studies demonstrate that basal autophagy in the kidney is vital for the normal homeostasis of the proximal tubules. Deletion of key autophagy proteins impaired renal function and increased p62 levels and oxidative stress. In models of AKI, autophagy deletion in proximal tubules worsened tubular injury and renal function, highlighting that autophagy is renoprotective in models of AKI. In addition to nonselective sequestration of autophagic cargo, autophagy can facilitate selective degradation of damaged organelles, particularly mitochondrial degradation through the process of mitophagy. Damaged mitochondria accumulate in autophagy-deficient kidneys of mice subjected to ischemia-reperfusion injury, but the precise mechanisms of regulation of mitophagy in AKI are not yet elucidated. Recent progress in identifying the interplay of autophagy, apoptosis, and regulated necrosis has revived interest in examining shared pathways/molecules in this crosstalk during the pathogenesis of AKI. Autophagy and its associated pathways pose potentially unique targets for therapeutic interventions in AKI.

Indexed as

AutophagyAcute Kidney InjuryAnimalsAntineoplastic AgentsApoptosisCaspasesCisplatinHumansLysosomesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesSepsisTOR Serine-Threonine KinasesAntineoplastic AgentsCaspasesCisplatinMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine Kinasesacute kidney injuryapoptosisautophagycell deathcisplatin nephrotoxicityischemia reperfusionmitophagy

Identifiers

PMID26924060
PMCPMC4801755
OpenAlexW2257214644

What OpenQuestion holds

Textmetadata
LicenceTDM
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.