Evidence map›Paper›PMID 27137489›Full record

ArticleEMBO molecular medicine2016

Chronic miR-29 antagonism promotes favorable plaque remodeling in atherosclerotic mice.

Victoria Ulrich, Noemi Rotllan, Elisa Araldi, Amelia Luciano, Philipp Skroblin, Mélanie Abonnenc, Paola Perrotta, Xiaoke Yin, Ashley Bauer, Kristen L Leslie and 9 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.8field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  9. Article
  10. Cellular crosstalk in atherosclerotic plaque microenvironment.Cell communication and signaling : CCS · 2023
    Review
  11. Article
  12. Review
  13. Broad-acting therapeutic effects of miR-29b-chitosan on hypertension and diabetic complications.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  14. Review
  15. MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022
    Review
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  18. Article
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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

19 authors at 4 institutions in 3 countries.

Victoria UlrichVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA.
Noemi RotllanVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine and Department of Pathology, School of Medicine Yale University, New Haven, CT, USA.
Elisa AraldiVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine and Department of Pathology, School of Medicine Yale University, New Haven, CT, USA.
Amelia LucianoVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA.
Philipp SkroblinKing's British Heart Foundation Centre, King's College London, London, UK.
Mélanie AbonnencKing's British Heart Foundation Centre, King's College London, London, UK.
Paola PerrottaVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA.
Xiaoke YinKing's British Heart Foundation Centre, King's College London, London, UK.
Ashley BauerVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Cardiology, School of Medicine Yale University, New Haven, CT, USA.
Kristen L LeslieVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Cardiology, School of Medicine Yale University, New Haven, CT, USA.
Pei ZhangVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA.
Binod AryalVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine and Department of Pathology, School of Medicine Yale University, New Haven, CT, USA.
Rusty L MontgomerymiRagen Therapeutics, Boulder, CO, USA.
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, Hannover, Germany National Heart and Lung Institute, Imperial College London, London, UK.
Kathleen MartinVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Cardiology, School of Medicine Yale University, New Haven, CT, USA.
Yajaira SuarezVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine and Department of Pathology, School of Medicine Yale University, New Haven, CT, USA.
Manuel MayrKing's British Heart Foundation Centre, King's College London, London, UK.
Carlos Fernandez-HernandoVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine and Department of Pathology, School of Medicine Yale University, New Haven, CT, USA.
William C SessaVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA Department of Pharmacology, School of Medicine Yale University, New Haven, CT, USA william.sessa@yale.edu.ORCID 0000-0001-5759-1938
Yale University · USKing's College London · GBMedizinische Hochschule Hannover · DEMiragen Therapeutics (United States) · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI MEGAN C KING · 1985 to 2026
$85.0M
PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Novel targets of rapamycin and Akt in vascular smooth muscle cell differentiationR01HL091013 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2008 to 2017
$4.1M
Regulation of vascular remodeling &angiogenesis by NogoR01HL081190 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2005 to 2014
$4.1M
microRNAs in vascular diseasesR01HL105945 · NHLBI · YALE UNIVERSITY · PI SUAREZ, YAJAIRA · 2011 to 2020
$3.7M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
Caveolin-1 in Lipoprotein Metabolism and Atherosclerosis.R01HL106063 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.5M
Role of microRNAs in lipid metabolism and cardiovascular diseaseR01HL107953 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2011 to 2016
$2.4M
Regulation of vascular smooth muscle cell plasticityR01HL118430 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2014 to 2017
$1.7M
Epigenetic control of vascular smooth muscle in cardiovascular diseaseR01HL119529 · NHLBI · YALE UNIVERSITY · PI MARTIN, KATHLEEN ANN · 2014 to 2017
$1.7M
British Heart Foundation FS/13/2/29892British Heart Foundation SP/12/5/29574NCI NIH HHS P30 CA016359NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL081190NHLBI NIH HHS R01 HL091013NHLBI NIH HHS R01 HL105945NHLBI NIH HHS R01 HL106063NHLBI NIH HHS R01 HL107953NHLBI NIH HHS R01 HL118430NHLBI NIH HHS R01 HL119529
6 · The paper itself

Abstract

Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chronic administration of LNA-miR-29 into an atherosclerotic mouse model improves indices of plaque morphology. This occurs due to upregulation of miR-29 target genes of the ECM (col1A and col3A) resulting in reduced lesion size, enhanced fibrous cap thickness, and reduced necrotic zones. Sustained LNA-miR-29 treatment did not affect circulating lipids, blood chemistry, or ECM of solid organs including liver, lung, kidney, spleen, or heart. Collectively, these data support the idea that antagonizing miR-29 may promote beneficial plaque remodeling as an independent approach to stabilize vulnerable atherosclerotic lesions.

Indexed as

AnimalsAtherosclerosisCollagen Type ICollagen Type I, alpha 1 ChainCollagen Type IIIDisease Models, AnimalMiceMicroRNAsCOL3A1 protein, mouseCollagen Type ICollagen Type I, alpha 1 ChainCollagen Type IIIMicroRNAsMIRN29 microRNA, mouseatherosclerosisLNAmiR‐29plaquestability

Identifiers

PMID27137489
PMCPMC4888854
OpenAlexW2344659999

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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.