Evidence map›Paper›PMID 26724508›Full record

ReviewThe Canadian journal of cardiology2016

Structure of the Elastin-Contractile Units in the Thoracic Aorta and How Genes That Cause Thoracic Aortic Aneurysms and Dissections Disrupt This Structure.

Ashkan Karimi, Dianna M Milewicz

Open access · greenAbstract readReview
In one paragraph

Review in The Canadian journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

98 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Fibronectin-induced overactivation of αNature communications · 2026
    Article
  6. Review
  7. Article
  8. Article
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  10. Review
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  14. Review
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  18. Inducing hypertension inFrontiers in cardiovascular medicine · 2025
    Article
  19. Article
  20. Review

38 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Ashkan KarimiDivision of Cardiovascular Medicine, Department of Medicine, University of Florida and the Division of Medical Genetics, Department of Internal Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Dianna M MilewiczDivision of Cardiovascular Medicine, Department of Medicine, University of Florida and the Division of Medical Genetics, Department of Internal Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA. Electronic address: Dianna.M.Milewicz@uth.tmc.edu.
The University of Texas Health Science Center at Houston · US

Funding

Pathology and Molecular Imaging CoreP01HL110869 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2012 to 2016
$10.4M
Genetic Predisposition To Thoracic Aortic Aneurysms/DissectionsR01HL109942 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2012 to 2023
$7.5M
Genetic Basis of Aortic Aneurysms/DissectionsR01HL062594 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MILEWICZ, DIANNA M · 2002 to 2009
$3.2M
NHLBI NIH HHS P01 HL110869NHLBI NIH HHS P01HL110869-01NHLBI NIH HHS R01 HL109942NHLBI NIH HHS R01 HL62594
6 · The paper itself

Abstract

The medial layer of the aorta confers elasticity and strength to the aortic wall and is composed of alternating layers of smooth muscle cells (SMCs) and elastic fibres. The SMC elastin-contractile unit is a structural unit that links the elastin fibres to the SMCs and is characterized by the following: (1) layers of elastin fibres that are surrounded by microfibrils; (2) microfibrils that bind to the integrin receptors in focal adhesions on the cell surface of the SMCs; and (3) SMC contractile filaments that are linked to the focal adhesions on the inner side of the membrane. The genes that are altered to cause thoracic aortic aneurysms and aortic dissections encode proteins involved in the structure or function of the SMC elastin-contractile unit. Included in this gene list are the genes encoding protein that are structural components of elastin fibres and microfibrils, FBN1, MFAP5, ELN, and FBLN4. Also included are genes that encode structural proteins in the SMC contractile unit, including ACTA2, which encodes SMC-specific α-actin and MYH11, which encodes SMC-specific myosin heavy chain, along with MYLK and PRKG1, which encode kinases that control SMC contraction. Finally, mutations in the gene encoding the protein linking integrin receptors to the contractile filaments, FLNA, also predispose to thoracic aortic disease. Thus, these data suggest that functional SMC elastin-contractile units are important for maintaining the structural integrity of the aorta.

Indexed as

VasoconstrictionAnimalsAorta, ThoracicAortic Aneurysm, ThoracicAortic DissectionDNAElastinGenotypeHumansMuscle, Smooth, VascularPhenotypeDNAElastin

Identifiers

PMID26724508
PMCPMC4839280
OpenAlexW2115839871

What OpenQuestion holds

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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.