Evidence map›Paper›PMID 24346810›Full record

ArticleJournal of psychopharmacology (Oxford, England)2014

Endothelial nitric oxide synthetase genetic variants, metabolic syndrome and endothelial function in schizophrenia.

Kj Burghardt, Tb Grove, Vl Ellingrod

Abstract read
In one paragraph

Article in Journal of psychopharmacology (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  14. Oxytocin ReceptorMolecular neuropsychiatry · 2016
    Article
  15. Role of Immune and Autoimmune Dysfunction in Schizophrenia.Handbook of behavioral neuroscience · 2016
    Article
  16. Review
  17. Article
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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.

Kj Burghardt1Department of Clinical Social and Administrative Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI, USA.
Tb Grove
Vl Ellingrod
University of Michigan–Ann Arbor · US

Funding

MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Folate Pharmacogenomics and Risk of Atypical Antipsychtoic Metabolic Side EffectsR01MH082784 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELLINGROD, VICKI L · 2008 to 2017
$4.0M
Genetics of Antipsychotic MetabolismK08MH064158 · NIMH · UNIVERSITY OF IOWA · PI ELLINGROD, VICKI L · 2001 to 2005
$743k
NCRR NIH HHS UL1 RR024986NCRR NIH HHS UL1RR024986NIDDK NIH HHS 5P60DK20572NIDDK NIH HHS P60 DK020572NIMH NIH HHS 2R01MH082784NIMH NIH HHS K08 MH064158NIMH NIH HHS R01 MH082784NIMH NIH HHS R01MH082784
6 · The paper itself

Abstract

objectiveThe increasing rates of metabolic syndrome and cardiovascular disease in schizophrenia led to investigation into their causes, including atypical antipsychotics and pharmacogenetic variants. This study focused on the peripheral vasculature as a cardiovascular phenotype and the influence of atypical antipsychotics, the aberrant metabolism of nitric oxide caused by endothelial nitric oxide synthetase (eNOS) genetic variants and metabolic syndrome in a cross-sectional sample of schizophrenia subjects.

methodsAssociations between eNOS genetic variants and endothelial function was assessed in a cohort of schizophrenia patients taking antipsychotic drugs, whom were undergoing a clinical assessment for endothelial function via the method of peripheral artery tonometry (RH-PAT), as well as metabolic syndrome criteria screening. Analyses were conducted on the entire cohort, then again after stratifying by metabolic syndrome, to investigate the effect of the eNOS variants and metabolic syndrome on endothelial functionality.

resultsWe included 203 subjects with a mean age of 46 years. The cohort was 36% female, 36% had metabolic syndrome and 85% were currently using atypical antipsychotics. We found associations between the eNOS T⁻⁷⁸⁶C and worse endothelial functioning (lower RH-PAT values) only in schizophrenia patients without metabolic syndrome.

conclusionsOur results suggested that when schizophrenia patients progress to meet metabolic syndrome criteria, the genetic protection of the eNOS T⁻⁷⁸⁶C variant on endothelial function is no longer seen: Other factors of this pro-inflammatory state may be overriding this effect. The results of this study need replication and the factors driving endothelial dysfunction in patients with metabolic syndrome warrant further investigation.

Indexed as

AdultAntipsychotic AgentsCross-Sectional StudiesDisease ProgressionEndothelium, VascularFemaleHumansMaleManometryMetabolic SyndromeMiddle AgedNitric OxideNitric Oxide Synthase Type IIIPharmacogeneticsRisk FactorsSchizophreniaAntipsychotic AgentsNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanAntipsychotic drugsendothelial cellsendothelial functioninflammationmetabolic syndromenitric oxide synthetaseperipheral artery tonometrypharmacogeneticsschizophrenia

Identifiers

PMID24346810
PMCPMC4039171
OpenAlexW2120357906

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.