Evidence map›Paper›PMID 38763809›Full record

ArticleJournal of biomechanics2024

Multiscale computational model of aortic remodeling following postnatal disruption of TGFβ signaling.

Ana C Estrada, Linda Irons, George Tellides, Jay D Humphrey

Abstract read
In one paragraph

Article in Journal of biomechanics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Ascending aortic aneurysm growth in the Fbln4Biomechanics and modeling in mechanobiology · 2025
    Article
  2. Article
  3. Article
  4. Transforming growth factor-beta (TGF-β) in the pathogenesis of hereditary thoracic aneurysm disorders.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    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

4 authors.

Ana C EstradaDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.
Linda IronsDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA.
George TellidesDepartment of Surgery, Cardiothoracic, Yale School of Medicine, New Haven, CT, USA; Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT, USA.
Jay D HumphreyDepartment of Biomedical Engineering, Yale University, New Haven, CT, USA; Vascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT, USA. Electronic address: jay.humphrey@yale.edu.

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Smooth Muscle Cell Proliferation and Degradative Phenotype in Thoracic Aorta Aneurysm and DissectionR01HL146723 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., TELLIDES, GEORGE · 2019 to 2022
$2.9M
Modeling Multiscale Immuno-Mechanics in Aortic DiseaseR01HL155105 · NHLBI · YALE UNIVERSITY · PI HUMPHREY, JAY D., TELLIDES, GEORGE · 2022 to 2025
$2.0M
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL146723NHLBI NIH HHS R01 HL155105
6 · The paper itself

Abstract

The healthy adult aorta is a remarkably resilient structure, able to resist relentless cardiac-induced and hemodynamic loads under normal conditions. Fundamental to such mechanical homeostasis is the mechano-sensitive cell signaling that controls gene products and thus the structural integrity of the wall. Mouse models have shown that smooth muscle cell-specific disruption of transforming growth factor-beta (TGFβ) signaling during postnatal development compromises this resiliency, rendering the aortic wall susceptible to aneurysm and dissection under normal mechanical loading. By contrast, disruption of such signaling in the adult aorta appears to introduce a vulnerability that remains hidden under normal loading, but manifests under increased loading as experienced during hypertension. We present a multiscale (transcript to tissue) computational model to examine possible reasons for compromised mechanical homeostasis in the adult aorta following reduced TGFβ signaling in smooth muscle cells.

Indexed as

AortaModels, CardiovascularSignal TransductionTransforming Growth Factor betaVascular RemodelingAnimalsComputer SimulationHumansMiceMyocytes, Smooth MuscleTransforming Growth Factor betaAortaBiomechanicsCell signalingHypertensionLogic-basedTransforming growth factor

Identifiers

PMID38763809
PMCPMC11141772

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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.