Evidence map›Paper›PMID 30971724›Full record

ArticleScientific reports2019

Distinct Phenotypes Induced by Three Degrees of Transverse Aortic Constriction in Mice.

Daniel A Richards, Mark J Aronovitz, Timothy D Calamaras, Kelly Tam, Gregory L Martin, Peiwen Liu, Heather K Bowditch, Phyllis Zhang, Gordon S Huggins, Robert M Blanton

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 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
24.8field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
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45 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Daniel A RichardsMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.ORCID http://orcid.org/0000-0002-9097-9325
Mark J AronovitzMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Timothy D CalamarasMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Kelly TamMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Gregory L MartinMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Peiwen LiuSackler School of Graduate Biomedical Sciences, Tufts University, 145 Harrison Avenue, Boston, MA, 02111, United States.
Heather K BowditchMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Phyllis ZhangMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Gordon S HugginsMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA.
Robert M BlantonMolecular Cardiology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, Massachusetts, 02111, USA. rblanton@tuftsmedicalenter.org.
Tufts Medical Center · USTufts University · US

Funding

Novel Protein Kinase GI Substrates in Cardiac Remodeling and Blood Pressure ControlR01HL131831 · NHLBI · TUFTS MEDICAL CENTER · PI BLANTON, ROBERT MORRIS · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL131831
6 · The paper itself

Abstract

Transverse aortic constriction (TAC) is a well-established model of pressure overload-induced cardiac hypertrophy and failure in mice. The degree of constriction "tightness" dictates the TAC severity and is determined by the gauge (G) of needle used. Though many reports use the TAC model, few studies have directly compared the range of resulting phenotypes. In this study adult male mice were randomized to receive TAC surgery with varying degrees of tightness: mild (25G), moderate (26G) or severe (27G) for 4 weeks, alongside sham-operated controls. Weekly echocardiography and terminal haemodynamic measurements determined cardiac remodelling and function. All TAC models induced significant, severity-dependent left ventricular hypertrophy and diastolic dysfunction compared to sham mice. Mice subjected to 26G TAC additionally exhibited mild systolic dysfunction and cardiac fibrosis, whereas mice in the 27G TAC group had more severe systolic and diastolic dysfunction, severe cardiac fibrosis, and were more likely to display features of heart failure, such as elevated plasma BNP. We also observed renal atrophy in 27G TAC mice, in the absence of renal structural, functional or gene expression changes. 25G, 26G and 27G TAC produced different responses in terms of cardiac structure and function. These distinct phenotypes may be useful in different preclinical settings.

Indexed as

Disease Models, AnimalAnimalsAorta, ThoracicConstriction, PathologicFibrosisHeart FailureHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMyocardiumPhenotypeRandom AllocationVentricular Dysfunction, Left

Identifiers

PMID30971724
PMCPMC6458135
OpenAlexW2938917295

What Socratic 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 Socratic graph.