Evidence map›Paper›PMID 22584609›Full record

ArticleBiomechanics and modeling in mechanobiology2012

Extracellular matrix and the mechanics of large artery development.

Jeffrey K Cheng, Jessica E Wagenseil

Open access · greenAbstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Multiscale insights into postnatal aortic development.Biomechanics and modeling in mechanobiology · 2024
    Article
  4. Article
  5. Developmental origins of mechanical homeostasis in the aorta.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  6. Longitudinal histomechanical heterogeneity of the internal thoracic artery.Journal of the mechanical behavior of biomedical materials · 2021
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Engineering of arteries in vitro.Cellular and molecular life sciences : CMLS · 2014
    Review
  18. Review
  19. Review
  20. Article
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 2 countries.

Jeffrey K ChengDepartment of Biomedical Engineering, Washington University, St. Louis, MO 63103, USA.
Jessica E Wagenseil
Saint Louis University · US

Funding

CARDIOVASCULAR SYSTEM--FUNCTION/REGULATION/PHARMACOLOGYT32HL007275 · NHLBI · WASHINGTON UNIVERSITY · PI NERBONNE, JEANNE M. · 1985 to 2013
$6.0M
VESSEL STIFFENING, HYPERTENSION, AND VASCULAR EXTRACELLULAR MATRIXR01HL105314 · NHLBI · WASHINGTON UNIVERSITY · PI MECHAM, ROBERT P., WAGENSEIL, JESSICA · 2010 to 2018
$3.2M
Mechanical Signals in Vessel DevelopmentR00HL087563 · NHLBI · SAINT LOUIS UNIVERSITY · PI WAGENSEIL, JESSICA · 2009 to 2011
$747k
NHLBI NIH HHS R00 HL087563NHLBI NIH HHS R01 HL105314NHLBI NIH HHS T32 HL007275
6 · The paper itself

Abstract

The large, elastic arteries, as their name suggests, provide elastic distention and recoil during the cardiac cycle in vertebrate animals. The arteries are distended from the pressure of ejecting blood during the active contraction of the left ventricle (LV) during systole and recoil to their original dimensions during relaxation of the LV during diastole. The cyclic distension occurs with minimal energy loss, due to the elastic properties of one of the major structural extracellular matrix (ECM) components, elastin. The maximum distension is limited to prevent damage to the artery by another major ECM component, collagen. The mix of ECM components in the wall largely determines the passive mechanical behavior of the arteries and the subsequent load on the heart during systole. While much research has focused on initial artery formation, there has been less attention on the continuing development of the artery to produce the mature composite wall complete with endothelial cells (ECs), smooth muscle cells (SMCs), and the necessary mix of ECM components for proper cardiovascular function. This review focuses on the physiology of large artery development, including SMC differentiation and ECM production. The effects of hemodynamic forces and ECM deposition on the evolving arterial structure and function are discussed. Human diseases and mouse models with genetic mutations in ECM proteins that affect large artery development are summarized. A review of constitutive models and growth and remodeling theories is presented, along with future directions to improve understanding of ECM and the mechanics of large artery development.

Indexed as

Models, BiologicalAnimalsArteriesComputer SimulationEmbryonic DevelopmentExtracellular MatrixHumansMechanotransduction, CellularMiceModels, AnimalStress, Mechanical

Identifiers

PMID22584609
PMCPMC3463721
OpenAlexW2076509587

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.