Evidence map›Paper›PMID 23276953›Full record

ArticleFrontiers in bioscience (Landmark edition)2013

Homocysteine induces inflammatory transcriptional signaling in monocytes.

Shu Meng, Stephen Ciment, Michael Jan, Tran Tran, Hung Pham, Ramon Cueto, Xiao-Feng Yang, Hong Wang

Open access · bronzeAbstract read
In one paragraph

Article in Frontiers in bioscience (Landmark edition), 2013. 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
3.5field-weighted citation impact, top 8% 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, 41 citations in OpenAlex.

  1. Article
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  14. Review
  15. Article
  16. Hyperhomocysteinemia Exacerbates Cisplatin-induced Acute Kidney Injury.International journal of biological sciences · 2017
    Article
  17. Article
  18. Analysis for Carom complex, signaling and function by database mining.Frontiers in bioscience (Landmark edition) · 2016
    Article
  19. Article
  20. Association of homocysteine with type 1 diabetes mellitus: a meta-analysis.International journal of clinical and experimental medicine · 2015
    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

8 authors at 1 institution in 1 country.

Shu MengDepartment of Pharmacology, Temple University School of Medicine, 3500 North Broad Street, 10th floor, Philadelphia, PA 19140, USA.
Stephen Ciment
Michael Jan
Tran Tran
Hung Pham
Ramon Cueto
Xiao-Feng Yang
Hong Wang
Temple University · US

Funding

Atherogenic mechanisms with homocysteineR01HL077288 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2004 to 2014
$3.8M
Inhibition of Endothelial Growth by HomocysteineR01HL067033 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2002 to 2011
$3.0M
Hyperhomocysteinemia and HDL MetabolismR01HL117654 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2013 to 2017
$3.0M
NADHP Oxidase-mediated MC differentiation & Endothelial Dysfunction in HHcyR01HL110764 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2011 to 2015
$2.5M
Roles of Interleukin-17 in Endothelial CellsR01HL108910 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2011 to 2015
$1.9M
Suppression of vascular endothelial cell inflammationR01HL094451 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2009 to 2013
$1.8M
Role of HHcy in diabetic vascular diseaseR01HL082774 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2006 to 2010
$1.8M
NHLBI NIH HHS HL108910NHLBI NIH HHS HL11076NHLBI NIH HHS HL67033NHLBI NIH HHS HL77288NHLBI NIH HHS HL82774NHLBI NIH HHS HL94451NHLBI NIH HHS R01 HL077288NHLBI NIH HHS R01 HL094451NHLBI NIH HHS R01 HL108910NHLBI NIH HHS R01 HL110764NHLBI NIH HHS R01 HL117654
6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease. Here, we studied transcriptional regulation in homocysteine (Hcy)-induced gene expression in monocytes (MC). We identified 11 Hcy-induced genes, 17 anti-inflammatory cytokine interleukin 10-induced, 8 pro-inflammatory cytokine interferon gamma (IFN gamma)-induced and 8 pro-inflammatory cytokine tumor necrosis factor alpha (TNF alpha)-induced genes through literature search. Binding frequency of 36 transcription factors (TFs) implicated in inflammation and MC differentiation were analyzed within core promoter regions of identified genes, and classified into 3 classes based on the significant binding frequency to the promoter of Hcy-induced genes. Class 1 TFs exert high significant binding frequency in Hcy-induced genes. Class 2 and 3 TFs have low and no significant binding frequency, respectively. Class 1 TF binding occurrence in Hcy-induced genes is similar to that in IFN gamma -induced genes, but not that in TNF alpha -induced. We conclude that Hcy is a pro-inflammatory amino acid and induces inflammatory transcriptional signal pathways mediated by class 1 TF. We term class 1 TF as putative Hcy-responsive TFs.

Indexed as

Cell DifferentiationCytokinesGene Expression RegulationHomocysteineHumansHyperhomocysteinemiaInterferon-gammaInterleukin-10MonocytesPromoter Regions, GeneticSignal TransductionTranscription FactorsCytokinesHomocysteineInterferon-gammaInterleukin-10Transcription Factors

Identifiers

PMID23276953
PMCPMC3636574
OpenAlexW2090138962

What OpenQuestion holds

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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.