Evidence map›Paper›PMID 30412443›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2019

Central artery stiffness and thoracic aortopathy.

J D Humphrey, G Tellides

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Hypertension drives thoracic aortic aneurysm and dissection in male, but not female, Marfan mice.Journal of the mechanical behavior of biomedical materials · 2026
    Article
  2. Mechanisms driving thoracic aortic aneurysm instability.Biomechanics and modeling in mechanobiology · 2026
    Article
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  17. Editorial: Advances in aortic imaging.Frontiers in cardiovascular medicine · 2023
    Article
  18. Article
  19. MicroRNAs in Mechanical Homeostasis.Cold Spring Harbor perspectives in medicine · 2022
    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 1 country.

J D HumphreyDepartment of Biomedical Engineering, Yale University , New Haven, Connecticut.ORCID 0000-0003-1011-2025
G TellidesDepartment of Surgery, Yale University , New Haven, Connecticut.
Yale University · US

Funding

TGFB-Dependent Mechanoresponses by Aortic Smooth Muscle Cells Govern AneurysmsP01HL134605 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RIFKIN, DANIEL B · 2018 to 2022
$12.1M
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
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
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
A new paradigm for aortic dissection: Mechanical mechanisms of delaminationR21EB020968 · NIBIB · YALE UNIVERSITY · PI HUMPHREY, JAY D. · 2016 to 2017
$461k
NHLBI NIH HHS P01 HL134605NHLBI NIH HHS R01 HL086418NHLBI NIH HHS R01 HL105297NHLBI NIH HHS R01 HL146723NHLBI NIH HHS U01 HL116323NHLBI NIH HHS U01 HL142518NIBIB NIH HHS R21 EB020968
6 · The paper itself

Abstract

Thoracic aortopathy, especially aneurysm, dissection, and rupture, is responsible for significant morbidity and mortality. Uncontrolled hypertension and aging are primary risk factors for such conditions, and they contribute to an increase in the mechanical stress on the wall and an increase in its structural vulnerability, respectively. Select genetic mutations also predispose to these lethal conditions, and the collection of known mutations suggests that dysfunctional mechanosensing and mechanoregulation of the extracellular matrix may contribute to pathogenesis and disease progression. In the absence of a well-accepted pharmacotherapy, nonsurgical treatments tend to focus on reducing the mechanical loading on the aorta, particularly via the use of antihypertensive medications and recommendations to avoid strenuous exercises such as weight lifting. In this brief review, we discuss the important effects of central artery stiffening on global hemodynamics and, in particular, on the increase in pulse pressure that acts on the proximal thoracic aorta. We consider Marfan syndrome as an illustrative aortopathy but discuss other conditions leading to thoracic aortic aneurysm and dissection. We highlight the importance of phenotyping the aorta biomechanically, not just clinically, and emphasize the utility of mouse models in elucidating molecular and mechanical mechanisms of disease. Notwithstanding the widely recognized role of central artery stiffening in driving end-organ disease, we suggest that there is similarly a need to consider its key role in thoracic aortopathy.

Indexed as

Vascular StiffnessAnimalsAorta, ThoracicAortic Aneurysm, ThoracicHumansMarfan Syndromeaortic aneurysmbiomechanical phenotypedissectionelastopathyhemodynamicsmechanotransduction

Identifiers

PMID30412443
PMCPMC6880196
OpenAlexW2899946397

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.