Evidence map›Paper›PMID 32068640›Full record

ArticleJournal of hypertension2020

Aortic remodeling is modest and sex-independent in mice when hypertension is superimposed on aging.

Bart Spronck, Jacopo Ferruzzi, Chiara Bellini, Alexander W Caulk, Sae-Il Murtada, Jay D Humphrey

Open access · hybridAbstract read
In one paragraph

Article in Journal of hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  11. Sex differences in vascular aging and impact of GPER deletion.American journal of physiology. Heart and circulatory physiology · 2022
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  18. Complementary roles of mechanotransduction and inflammation in vascular homeostasis.Proceedings. Mathematical, physical, and engineering sciences · 2021
    Article
  19. 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

6 authors at 3 institutions in 2 countries.

Bart SpronckDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Jacopo FerruzziDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Chiara BelliniDepartment of Bioengineering, Northeastern University, Boston, Massachusetts.
Alexander W CaulkDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Sae-Il MurtadaDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Jay D HumphreyDepartment of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Yale University · USMaastricht University · NLNortheastern 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
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 HL105297ZonMw 452172006
6 · The paper itself

Abstract

objectivesIncreased central artery stiffness associates with cardiovascular disease. Among other factors, hypertension and aging are strong contributors to central artery stiffening, yet it has been difficult to separate their effects. Herein, we study isolated and combined effects of hypertension and aging on central artery remodeling in multiple mouse models as a function of sex.

methodsWe biomechanically phenotyped the aorta as a function of two different methods of inducing hypertension [infusion of angiotensin II (AngII) or combining a high salt diet with inhibition of endothelial-derived nitric oxide synthase using L-NAME] in male and female wild-type and fibulin-5 null mice, the latter of which models aspects of aortic aging.

resultsDespite increasing blood pressure similarly, salt + L-NAME led to adaptive and maladaptive remodeling in the abdominal and thoracic aorta, respectively, whereas AngII caused luminal dilatation but little remodeling of the wall. Importantly, effects of aging were more dramatic than those resulting from induced hypertension and, consequently, superimposing hypertension on aging led to modest additional changes in luminal radius and wall thickness, though wall stress and stiffness increased mainly because of the elevated pressure.

conclusionOur results suggest that effects of hypertension on aortic remodeling are modest when superimposed on aging in mice, largely independent of sex. These findings are consistent with general observations in humans and in spontaneously hypertensive rats, though separated here for the first time in a rodent model characterized by a severe loss of elastic fiber integrity similar to that found in the aged human aorta.

Indexed as

AgingAngiotensin IIAnimalsAortaAorta, AbdominalAorta, ThoracicFemaleHemodynamicsHypertensionMaleMiceNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIPhenotypeSodium Chloride, DietaryAngiotensin IING-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIINos3 protein, mouseSodium Chloride, Dietary

Identifiers

PMID32068640
PMCPMC7611466
OpenAlexW3008827944

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.