Evidence map›Paper›PMID 24896770›Full record

ArticlePloS one2014

Sirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injury.

Rong Gao, Jiao Chen, Yuxin Hu, Zhenyu Li, Shuxia Wang, Sreerama Shetty, Jian Fu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 72 citations in OpenAlex.

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  16. Article
  17. Sirtuin 5 Regulates Proximal Tubule Fatty Acid Oxidation to Protect against AKI.Journal of the American Society of Nephrology : JASN · 2019
    Article
  18. Article
  19. Sirtuin-1 in immunotherapy: A Janus-headed target.Journal of leukocyte biology · 2019
    Review
  20. Article
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 2 institutions in 2 countries.

Rong GaoThe Second Hospital of Jilin University, Changchun, Jilin, China; Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Jiao ChenCenter for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Yuxin HuThe Second Hospital of Jilin University, Changchun, Jilin, China; Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Zhenyu LiDivision of Cardiovascular Medicine, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Shuxia WangGraduate Center for Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Sreerama ShettyCenter for Biomedical Research, University of Texas Health Science Center at Tyler, Tyler, Texas, United States of America.
Jian FuCenter for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America; Graduate Center for Toxicology, College of Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
University of Kentucky · USThe University of Texas Health Science Center at Tyler · US

Funding

Sirt1 regulation of NFkB activation and inflammatory responses in sepsisR01GM099744 · NIGMS · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI FU, JIAN · 2012 to 2016
$1.3M
NIGMS NIH HHS 1R01GM099744NIGMS NIH HHS R01 GM099744
6 · The paper itself

Abstract

Bacterial endotoxin has been known to induce excessive inflammatory responses and acute kidney injury. In the present study, we used a mouse model of endotoxemia to investigate the role of Sirt1 in inflammatory kidney injury. We examined molecular and cellular responses in inducible Sirt1 knockout (Sirt1-/-) mice and wild type littermates (Sirt1+/+) in lipopolysaccharide (LPS)-induced kidney injury. Our studies demonstrated that Sirt1 deletion caused aggravated kidney injury, which was associated with increased inflammatory responses including elevated pro-inflammatory cytokine production, and increased ICAM-1 and VCAM-1 expression. Inflammatory signaling such as STAT3/ERK phosphorylation and NF-κB activation was markedly elevated in kidney tissues of Sirt1 knockout mice after LPS challenge. The results indicate that Sirt1 is protective against LPS-induced acute kidney injury by suppressing kidney inflammation and down-regulating inflammatory signaling.

Indexed as

Gene DeletionAcute Kidney InjuryAnimalsDisease Models, AnimalDisease ProgressionEndotoxinsGene ExpressionInflammationIntercellular Adhesion Molecule-1Kidney TubulesLipopolysaccharidesMaleMiceMice, KnockoutNeutrophil InfiltrationSignal TransductionEndotoxinsIntercellular Adhesion Molecule-1LipopolysaccharidesSirtuin 1Vascular Cell Adhesion Molecule-1

Identifiers

PMID24896770
PMCPMC4045768
OpenAlexW2136650715

What OpenQuestion holds

Textmetadata
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.