Evidence map›Paper›PMID 27923220›Full record

ArticleJournal of vascular research2016

Differential Regulation of BMAL1, CLOCK, and Endothelial Signaling in the Aortic Arch and Ligated Common Carotid Artery.

Xia Shang, Paramita Pati, Ciprian B Anea, David J R Fulton, R Daniel Rudic

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of vascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% 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, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  17. Old and New Roles and Evolving Complexities of Cardiovascular Clocks.The Yale journal of biology and medicine · 2019
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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 1 institution in 1 country.

Xia ShangDepartment of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Paramita Pati
Ciprian B Anea
David J R Fulton
R Daniel Rudic
Augusta University · US

Funding

Novel mechanistic pathways of cardiovascular disease in obesityR01HL124773 · NHLBI · AUGUSTA UNIVERSITY · PI FULTON, DAVID J, STEPP, DAVID W · 2015 to 2018
$2.2M
The biological clock, the endothelium, and vascular remodelingR01HL089576 · NHLBI · AUGUSTA UNIVERSITY · PI RUDIC, RADU DANIEL · 2008 to 2012
$2.1M
NHLBI NIH HHS R01 HL089576NHLBI NIH HHS R01 HL124773
6 · The paper itself

Abstract

The circadian clock is rhythmically expressed in blood vessels, but the interaction between the circadian clock and disturbed blood flow remains unclear. We examined the relationships between BMAL1 and CLOCK and 2 regulators of endothelial function, AKT1 and endothelial nitric oxide synthase (eNOS), in vascular regions of altered blood flow. We found that the aortic arch from WT mice exhibited reduced sensitivity to acetylcholine (Ach)-mediated relaxation relative to the thoracic aorta. In Clock-mutant (mut) mice the aorta exhibited a reduced sensitivity to Ach. In WT mice, the phosphorylated forms of eNOS and AKT were decreased in the aortic arch, while BMAL1 and CLOCK expression followed a similar pattern of reduction in the arch. In conditions of surgically induced flow reduction, phosphorylated-eNOS (serine 1177) increased, as did p-AKT in the ipsilateral left common carotid artery (LC) of WT mice. Similarly, BMAL1 and CLOCK exhibited increased expression after 5 days in the remodeled LC. eNOS expression was increased at 8 p.m. versus 8 a.m. in WT mice, and this pattern was abolished in mut and Bmal1-KO mice. These data suggest that the circadian clock may be a biomechanical and temporal sensor that acts to coordinate timing, flow dynamics, and endothelial function.

Indexed as

Circadian RhythmMechanotransduction, CellularAnimalsAorta, ThoracicARNTL Transcription FactorsCarotid Artery DiseasesCarotid Artery, ExternalCLOCK ProteinsDisease Models, AnimalDose-Response Relationship, DrugGene Expression RegulationGenotypeLigationMaleMice, Inbred C57BLMice, KnockoutAkt1 protein, mouseARNTL Transcription FactorsBmal1 protein, mouseClock protein, mouseCLOCK ProteinsNitric Oxide Synthase Type IIINos3 protein, mouseProto-Oncogene Proteins c-aktVasodilator Agents

Identifiers

PMID27923220
PMCPMC5765856
OpenAlexW2559960586

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.