Evidence map›Paper›PMID 26837267›Full record

ArticleNature communications2016

Endothelial Dicer promotes atherosclerosis and vascular inflammation by miRNA-103-mediated suppression of KLF4.

Petra Hartmann, Zhe Zhou, Lucia Natarelli, Yuanyuan Wei, Maliheh Nazari-Jahantigh, Mengyu Zhu, Jochen Grommes, Sabine Steffens, Christian Weber, Andreas Schober

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
11.5field-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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
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  14. Vascular mechanotransduction.Physiological reviews · 2023
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Petra HartmannInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Zhe ZhouInstitute for Molecular Cardiovascular Research, RWTH Aachen University, Pauwelsstrasse 30, 52074 Aachen, Germany.
Lucia NatarelliInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Yuanyuan WeiInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Maliheh Nazari-JahantighInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Mengyu ZhuInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Jochen GrommesEuropean Vascular Center Aachen-Maastricht, Medical University Maastricht, P. Debyelaan 25, 6229 HX Maastricht, The Netherlands.
Sabine SteffensInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Christian WeberInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Andreas SchoberInstitute for Cardiovascular Prevention, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9, 80336 Munich, Germany.
Ludwig-Maximilians-Universität München · DERWTH Aachen University · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs regulate the maladaptation of endothelial cells (ECs) to naturally occurring disturbed blood flow at arterial bifurcations resulting in arterial inflammation and atherosclerosis in response to hyperlipidemic stress. Here, we show that reduced endothelial expression of the RNAse Dicer, which generates almost all mature miRNAs, decreases monocyte adhesion, endothelial C-X-C motif chemokine 1 (CXCL1) expression, atherosclerosis and the lesional macrophage content in apolipoprotein E knockout mice (Apoe(-/-)) after exposure to a high-fat diet. Endothelial Dicer deficiency reduces the expression of unstable miRNAs, such as miR-103, and promotes Krüppel-like factor 4 (KLF4)-dependent gene expression in murine atherosclerotic arteries. MiR-103 mediated suppression of KLF4 increases monocyte adhesion to ECs by enhancing nuclear factor-κB-dependent CXCL1 expression. Inhibiting the interaction between miR-103 and KLF4 reduces atherosclerosis, lesional macrophage accumulation and endothelial CXCL1 expression. Overall, our study suggests that Dicer promotes endothelial maladaptation and atherosclerosis in part by miR-103-mediated suppression of KLF4.

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisBlotting, WesternCarotid ArteriesCell AdhesionCells, CulturedChemokine CXCL1DEAD-box RNA HelicasesDiet, High-FatEndarterectomy, CarotidEndothelial CellsEnzyme-Linked Immunosorbent AssayGene Expression ProfilingHumansApolipoproteins EChemokine CXCL1CXCL1 protein, humanCxcl1 protein, mouseDEAD-box RNA HelicasesDICER1 protein, humanDicer1 protein, mouseKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN103 microRNA, humanMIRN103 microRNA, mouseNF-kappa BRibonuclease III

Identifiers

PMID26837267
PMCPMC4742841
OpenAlexW2301328440

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.