Evidence map›Paper›PMID 31653875›Full record

ArticleScientific reports2019

Modeling lamellar disruption within the aortic wall using a particle-based approach.

H Ahmadzadeh, M K Rausch, J D Humphrey

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Extrusion bioprinting: meeting the promise of human tissue biofabrication?Progress in biomedical engineering (Bristol, England) · 2025
    Review
  7. Hyperglycemia inhibits AAA expansion: examining the role of lysyl oxidase.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Differential propensity of dissection along the aorta.Biomechanics and modeling in mechanobiology · 2021
    Article
  17. Review
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 2 institutions in 1 country.

H AhmadzadehDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.
M K RauschDepartment of Aerospace Engineering and Engineering Mechanics, Department of Biomedical Engineering, University of Texas at Austin, Austin, TX, USA.
J D HumphreyDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA. jay.humphrey@yale.edu.ORCID http://orcid.org/0000-0003-1011-2025
Yale University · USThe University of Texas at Austin · US

Funding

TGFB-Dependent Mechanoresponses by Aortic Smooth Muscle Cells Govern AneurysmsP01HL134605 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUMPHREY, JAY D. · 2018 to 2022
$12.1M
Multimodality imaging-driven multifidelity modeling of aortic dissectionU01HL142518 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., KARNIADAKIS, GEORGE · 2018 to 2022
$2.8M
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 P01 HL134605NHLBI NIH HHS U01 HL116323NHLBI NIH HHS U01 HL142518
6 · The paper itself

Abstract

Aortic dissections associate with medial degeneration, thus suggesting a need to understand better the biophysical interactions between the cells and matrix that constitute the middle layer of the aortic wall. Here, we use a recently extended "Smoothed Particle Hydrodynamics" formulation to examine potential mechanisms of aortic delamination arising from smooth muscle cell (SMC) dysfunction or apoptosis, degradation of or damage to elastic fibers, and pooling of glycosaminoglycans (GAGs), with associated losses of medial collagen in the region of the GAGs. First, we develop a baseline multi-layered model for the healthy aorta that delineates medial elastic lamellae and intra-lamellar constituents. Next, we examine stress fields resulting from the disruption of individual elastic lamellae, lost SMC contractility, and GAG production within an intra-lamellar space, focusing on the radial transferal of loading rather than on stresses at the tip of the delaminated tissue. Results suggest that local disruptions of elastic lamellae transfer excessive loads to nearby intra-lamellar constituents, which increases cellular vulnerability to dysfunction or death. Similarly, lost SMC function and accumulations of GAGs increase mechanical stress on nearby elastic lamellae, thereby increasing the chance of disruption. Overall these results suggest a positive feedback loop between lamellar disruption and cellular dropout with GAG production and lost medial collagen that is more pronounced at higher distending pressures. Independent of the initiating event, this feedback loop can catastrophically propagate intramural delamination.

Indexed as

Models, CardiovascularStress, MechanicalAnimalsAortaApoptosisBiomechanical PhenomenaElasticityFeedbackGlycosaminoglycansHydrodynamicsMiceMyocytes, Smooth MuscleGlycosaminoglycans

Identifiers

PMID31653875
PMCPMC6814784
OpenAlexW2981680418

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.