Evidence map›Paper›PMID 24920112›Full record

ArticleJournal of the Royal Society, Interface2014

Computational modelling suggests good, bad and ugly roles of glycosaminoglycans in arterial wall mechanics and mechanobiology.

S Roccabianca, C Bellini, J D Humphrey

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Growth arrest of thoracic aortic aneurysms in aging Marfan mice.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  4. Mechanics and mechanobiology of arterial development.Biomechanics and modeling in mechanobiology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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  12. Article
  13. Review
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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

3 authors at 1 institution in 1 country.

S RoccabiancaDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.
C BelliniDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.
J D HumphreyDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT, USA jay.humphrey@yale.edu.
Yale University · US

Funding

Biomechanical Simulation of Evolving Aortic Aneurysms for Designing InterventionR01HL086418 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D. · 2008 to 2017
$3.8M
Mechanisms Underlying The Progression of Large Artery Stiffness in HypertensionR01HL105297 · NHLBI · YALE UNIVERSITY · PI FIGUEROA, CARLOS ALBERTO, HUMPHREY, JAY D. · 2010 to 2019
$3.0M
Multiscale, Multiphysics Model of Thrombus Biomechanics in Aortic DissectionU01HL116323 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., KARNIADAKIS, GEORGE · 2013 to 2017
$2.4M
NHLBI NIH HHS R01 HL086418NHLBI NIH HHS R01 HL105297NHLBI NIH HHS U01 HL116323
6 · The paper itself

Abstract

The medial layer of large arteries contains aggregates of the glycosaminoglycan hyaluronan and the proteoglycan versican. It is increasingly thought that these aggregates play important mechanical and mechanobiological roles despite constituting only a small fraction of the normal arterial wall. In this paper, we offer a new hypothesis that normal aggregates of hyaluronan and versican pressurize the intralamellar spaces, and thereby put into tension the radial elastic fibres that connect the smooth muscle cells to the elastic laminae, which would facilitate mechanosensing. This hypothesis is supported by novel computational simulations using two complementary models, a mechanistically based finite-element mixture model and a phenomenologically motivated continuum hyperelastic model. That is, the simulations suggest that normal aggregates of glycosaminoglycans/proteoglycans within the arterial media may play equally important roles in supporting (i.e. a structural role) and sensing (i.e. an instructional role) mechanical loads. Additional simulations suggest further, however, that abnormal increases in these aggregates, either distributed or localized, may over-pressurize the intralamellar units. We submit that these situations could lead to compromised mechanosensing, anoikis and/or reduced structural integrity, each of which represent fundamental aspects of arterial pathologies seen, for example, in hypertension, ageing and thoracic aortic aneurysms and dissections.

Indexed as

Mechanotransduction, CellularModels, CardiovascularAnimalsCarotid Artery, CommonCarotid Artery DiseasesComputer SimulationGlycosaminoglycansMiceProteoglycansShear StrengthStress, MechanicalTensile StrengthTunica IntimaGlycosaminoglycansProteoglycansanoikishyaluronanmechanosensingstress analysisversican

Identifiers

PMID24920112
PMCPMC4208372
OpenAlexW2039354854

What OpenQuestion holds

Textmetadata
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.