Evidence map›Paper›PMID 23042817›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Krüppel-like factor-11, a transcription factor involved in diabetes mellitus, suppresses endothelial cell activation via the nuclear factor-κB signaling pathway.

Yanbo Fan, Yanhong Guo, Jifeng Zhang, Malayannan Subramaniam, Chao-Zhong Song, Raul Urrutia, Y Eugene Chen

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

34 citing papers in PubMed, 46 citations in OpenAlex.

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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 2 institutions in 1 country.

Yanbo FanCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109, USA.
Yanhong Guo
Jifeng Zhang
Malayannan Subramaniam
Chao-Zhong Song
Raul Urrutia
Y Eugene Chen
Mayo Clinic in Arizona · USUniversity of Washington · US

Funding

The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
ZINC FINGER GENES AND PANCREATIC CELL GROWTHR01DK052913 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI LOMBERK, GWEN, URRUTIA, RAUL A. · 1998 to 2023
$7.0M
Nitro-Fatty Acids and Nrf2 in Vascular RemodelingR01HL105114 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2010 to 2014
$2.6M
Nitroalkenes and Blood Pressure RegulationR01HL089544 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2012
$2.0M
Nitroalkene-Mediated Vascular Protection and Ischemic StrokeR01NS066652 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2011 to 2014
$1.3M
The Role of Zinc Finger Genes in Pancreatic Cell GrowthR56DK052913 · NIDDK · MAYO CLINIC ROCHESTER · PI URRUTIA, RAUL A. · 2008 to 2008
$291k
NHLBI NIH HHS HL068878NHLBI NIH HHS HL089544NHLBI NIH HHS HL105114NHLBI NIH HHS R01 HL068878NHLBI NIH HHS R01 HL089544NHLBI NIH HHS R01 HL105114NIDDK NIH HHS DK52913NIDDK NIH HHS R01 DK052913NIDDK NIH HHS R56 DK052913NINDS NIH HHS R01 NS066652
6 · The paper itself

Abstract

objectiveEndothelial cell (EC) inflammatory status is critical to many vascular diseases. Emerging data demonstrate that mutations of Krüppel-like factor-11 (KLF11), a gene coding maturity-onset diabetes mellitus of the young type 7 (MODY7), contribute to the development of neonatal diabetes mellitus. However, the function of KLF11 in the cardiovascular system still remains to be uncovered. In this study, we aimed to investigate the role of KLF11 in vascular endothelial inflammation. METHODS AND

resultsKLF11 is highly expressed in vascular ECs and induced by proinflammatory stimuli. Adenovirus-mediated KLF11 overexpression inhibits expression of tumor necrosis factors-α-induced adhesion molecules. Moreover, small interfering RNA-mediated KLF11 knockdown augments the proinflammatory status in ECs. KLF11 inhibits promoter activity of adhesion molecules induced by tumor necrosis factor-α and nuclear factor-κB p65 overexpression. Mechanistically, KLF11 potently inhibits nuclear factor-κB signaling pathway via physical interaction with p65. Furthermore, KLF11 knockdown results in increased binding of p65 to vascular cell adhesion molecule-1 and E-selectin promoters. At the whole organism level, KLF11(-/-) mice exhibit a significant increase in leukocyte recruitment to ECs after lipopolysaccharide administration.

conclusionsTaken together, our data demonstrate for the first time that KLF11 is a suppressor of EC inflammatory activation, suggesting that KLF11 constitutes a novel potential molecular target for inhibition of vascular inflammatory diseases.

Indexed as

AnimalsApoptosis Regulatory ProteinsCell Cycle ProteinsCell LineDiabetes MellitusDNA-Binding ProteinseIF-2 KinaseEndothelium, VascularE-SelectinHumansLeukocytesLipopolysaccharidesMiceMice, KnockoutNF-kappa BProtein BindingApoptosis Regulatory ProteinsCell Cycle ProteinsDNA-Binding ProteinseIF-2 KinaseE-SelectinKLF11 protein, humanKLF11 protein, mouseLipopolysaccharidesNF-kappa BRepressor ProteinsRNA, Small InterferingTranscription FactorsVascular Cell Adhesion Molecule-1

Identifiers

PMID23042817
PMCPMC3556387
OpenAlexW2127316036

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.