Evidence map›Paper›PMID 24312398›Full record

ArticlePloS one2013

Smooth muscle LDL receptor-related protein-1 deletion induces aortic insufficiency and promotes vascular cardiomyopathy in mice.

Joshua E Basford, Sheryl Koch, Ahmad Anjak, Vivek P Singh, Eric G Krause, Nathan Robbins, Neal L Weintraub, David Y Hui, Jack Rubinstein

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Genetic Variation inJournal of cardiovascular development and disease · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

9 authors at 1 institution in 1 country.

Joshua E BasfordDepartment of Pathology, Metabolic Diseases Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.
Sheryl Koch
Ahmad Anjak
Vivek P Singh
Eric G Krause
Nathan Robbins
Neal L Weintraub
David Y Hui
Jack Rubinstein
University of Cincinnati Medical Center · US

Funding

Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2012 to 2014
$9.9M
Role of Lipoprotein Receptors in Diet-induced Obesity and DiabetesR01DK074932 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2007 to 2019
$4.4M
Angiotensin II, oxidative stress, and aneurysm formationR01HL076684 · NHLBI · UNIVERSITY OF IOWA · PI WEINTRAUB, NEAL L · 2005 to 2013
$3.0M
Perivascular adipose tissue and vascular remodelingR01HL112640 · NHLBI · UNIVERSITY OF CINCINNATI · PI WEINTRAUB, NEAL L · 2012 to 2016
$2.1M
NCATS NIH HHS UL1 TR000077NHLBI NIH HHS HL076684NHLBI NIH HHS R01 HL076684NHLBI NIH HHS R01 HL112640NIDDK NIH HHS DK074932NIDDK NIH HHS R01 DK074932
6 · The paper itself

Abstract

Valvular disease is common in patients with Marfan syndrome and can lead to cardiomyopathy. However, some patients develop cardiomyopathy in the absence of hemodynamically significant valve dysfunction, suggesting alternative mechanisms of disease progression. Disruption of LDL receptor-related protein-1 (Lrp1) in smooth muscle cells has been shown to cause vascular pathologies similar to Marfan syndrome, with activation of smooth muscle cells, vascular dysfunction and aortic aneurysms. This study used echocardiography and blood pressure monitoring in mouse models to determine whether inactivation of Lrp1 in vascular smooth muscle leads to cardiomyopathy, and if so, whether the mechanism is a consequence of valvular disease. Hemodynamic changes during treatment with captopril were also assessed. Dilation of aortic roots was observed in young Lrp1-knockout mice and progressed as they aged, whereas no significant aortic dilation was detected in wild type littermates. Diastolic blood pressure was lower and pulse pressure higher in Lrp1-knockout mice, which was normalized by treatment with captopril. Aortic dilation was followed by development of aortic insufficiency and subsequent dilated cardiomyopathy due to valvular disease. Thus, smooth muscle cell Lrp1 deficiency results in aortic dilation and insufficiency that causes secondary cardiomyopathy that can be improved by captopril. These findings provide novel insights into mechanisms of cardiomyopathy associated with vascular activation and offer a new model of valvular cardiomyopathy.

Indexed as

Gene DeletionAgingAnimalsAortic Valve InsufficiencyBlood PressureBlood VesselsCardiomyopathiesLow Density Lipoprotein Receptor-Related Protein-1MaleMAP Kinase Signaling SystemMiceMice, KnockoutMuscle, SmoothPhosphorylationSmad2 ProteinUltrasonographyLow Density Lipoprotein Receptor-Related Protein-1Smad2 ProteinSmad2 protein, mouse

Identifiers

PMID24312398
PMCPMC3843717
OpenAlexW1963565813

What OpenQuestion holds

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LicenceCC BY
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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.