Evidence map›Paper›PMID 29754316›Full record

ArticleBiomechanics and modeling in mechanobiology2018

Compromised mechanical homeostasis in arterial aging and associated cardiovascular consequences.

J Ferruzzi, D Madziva, A W Caulk, G Tellides, J D Humphrey

Open access · greenAbstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.7field-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

49 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Growth arrest of thoracic aortic aneurysms in aging Marfan mice.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Mechanics and mechanobiology of arterial development.Biomechanics and modeling in mechanobiology · 2026
    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

5 authors at 3 institutions in 1 country.

J FerruzziDepartment of Biomedical Engineering, Malone Engineering Center, Yale University, 55 Prospect Street, New Haven, CT, 06520, USA.
D MadzivaDepartment of Biomedical Engineering, Malone Engineering Center, Yale University, 55 Prospect Street, New Haven, CT, 06520, USA.
A W CaulkDepartment of Biomedical Engineering, Malone Engineering Center, Yale University, 55 Prospect Street, New Haven, CT, 06520, USA.
G TellidesVascular Biology and Therapeutics Program, Yale School of Medicine, New Haven, CT, USA.
J D HumphreyDepartment of Biomedical Engineering, Malone Engineering Center, Yale University, 55 Prospect Street, New Haven, CT, 06520, USA. jay.humphrey@yale.edu.ORCID http://orcid.org/0000-0003-1011-2025
Yale University · USBoston University · USYale Cancer Center · 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
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
NHLBI NIH HHS P01 HL134605NHLBI NIH HHS R01 HL105297NIH HHS R01 HL105297
6 · The paper itself

Abstract

Aging leads to central artery stiffening and associated hemodynamic sequelae. Because healthy arteries exhibit differential geometry, composition, and mechanical behaviors along the central vasculature, we sought to determine whether wall structure and mechanical function differ across five vascular regions-the ascending and descending thoracic aorta, suprarenal and infrarenal abdominal aorta, and common carotid artery-in 20 versus 100-week-old male wild-type mice. Notwithstanding generally consistent changes across these regions, including a marked thickening of the arterial wall, diminished in vivo axial stretch, and loss of elastic energy storage capacity, the degree of changes tended to be slightly greater in abdominal than in thoracic or carotid vessels. Likely due to the long half-life of vascular elastin, most mechanical changes in the arterial wall resulted largely from a distributed increase in collagen, including thicker fibers in the media, and localized increases in glycosaminoglycans. Changes within the central arteries associated with significant increases in central pulse pressure and adverse changes in the left ventricle, including increased cardiac mass and decreased diastolic function. Given the similar half-life of vascular elastin in mice and humans but very different life-spans, there are important differences in the aging of central vessels across these species. Nevertheless, the common finding of aberrant matrix remodeling contributing to a compromised mechanical homeostasis suggests that studies of central artery aging in the mouse can provide insight into mechanisms and treatment strategies for the many adverse effects of vascular aging in humans.

Indexed as

AgingHomeostasisAnimalsAorta, AbdominalAorta, ThoracicBiomechanical PhenomenaCardiovascular DiseasesCardiovascular SystemCarotid ArteriesCarotid Artery, CommonDiastoleDisease Models, AnimalElastinExtracellular Matrix ProteinsHemodynamicsHumansElastinExtracellular Matrix ProteinsFbln5 protein, mouseRecombinant ProteinsArterial stiffnessDiastolic functionElastic energyFibrosisVentricular hypertrophy

Identifiers

PMID29754316
PMCPMC8344131
OpenAlexW2801639838

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.