Evidence map›Paper›PMID 27374117›Full record

ArticleJournal of molecular and cellular cardiology2016

Vitamin D controls resistance artery function through regulation of perivascular adipose tissue hypoxia and inflammation.

Christopher J Pelham, Elizabeth M Drews, Devendra K Agrawal

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  19. Role of Vitamin D in Cardiovascular Diseases.Endocrinology and metabolism clinics of North America · 2017
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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

3 authors at 1 institution in 1 country.

Christopher J PelhamDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA.
Elizabeth M DrewsDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA.
Devendra K AgrawalDepartment of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA. Electronic address: dkagr@creighton.edu.
Creighton University · US

Funding

EPICARDIAL ADIPOSE TISSUE, OBESITY AND INFLAMMATION IN ATHEROSCLEROSISR01HL120659 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2013 to 2017
$3.6M
VITAMIN D AND IMMUNOMODULATION IN CORONARY ARTERY DISEASER01HL116042 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2012 to 2016
$3.3M
GENE THERAPY WITH SOCS-3 IN INTIMAL HYPERPLASIA AND IN-STENT RESTENOSISR01HL104516 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2011 to 2014
$2.4M
NHLBI NIH HHS R01 HL104516NHLBI NIH HHS R01 HL116042NHLBI NIH HHS R01 HL120659
6 · The paper itself

Abstract

Vitamin D deficiency in human subjects is associated with hypertension, metabolic syndrome and related risk factors of cardiovascular diseases. Serum 25-hydroxyvitamin D levels correlate inversely with adiposity in obese and lean individuals. Bioactive vitamin D, or calcitriol, exerts anti-inflammatory effects on adipocytes, preadipocytes and macrophages in vitro. We tested the hypothesis that vitamin D deficiency alters the phenotype of perivascular adipose tissue (PVAT) leading to impaired function in resistance artery. To examine the effects of vitamin D and PVAT on vascular reactivity, myograph experiments were performed on arteries, with or without intact PVAT, from mice maintained on vitamin D-deficient, vitamin D-sufficient or vitamin D-supplemented diet. Systolic blood pressure was significantly increased in mice on vitamin D-deficient diet. Importantly, vitamin D deficiency enhanced angiotensin II-induced vasoconstriction and impaired the normal ability of PVAT to suppress contractile responses of the underlying mesenteric resistance artery to angiotensin II and serotonin. Furthermore, vitamin D deficiency caused upregulation of the mRNA expression of tumor necrosis factor-α, hypoxia-inducible factor-1α and its downstream target lysyl oxidase in mesenteric PVAT. Incubation of mesenteric arteries under hypoxic conditions impaired the anti-contractile effects of intact PVAT on those arteries from mice on vitamin D-sufficient diet. Vitamin D supplementation protected arteries against hypoxia-induced impairment of PVAT function. The protective effects of vitamin D against vascular dysfunction, hypertension and cardiovascular diseases may be mediated, at least in part, through regulation of inflammatory and hypoxia signaling pathways in PVAT.

Indexed as

Vascular ResistanceAdipose TissueAnimal FeedAnimalsArteriesBlood PressureFemaleGene Expression ProfilingHypoxiaInflammationMaleMesenteric ArteriesMiceMuscle ContractionPhenotypeVitamin DVitamin DHypoxiaInflammationPerivascular adipose tissueResistance arteryVitamin D

Identifiers

PMID27374117
PMCPMC5026596
OpenAlexW2472484948

What Socratic 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 Socratic graph.