Evidence map›Paper›PMID 17982132›Full record

ArticleThe American journal of pathology2007

Reactive aldehyde modification of thioredoxin-1 activates early steps of inflammation and cell adhesion.

Young-Mi Go, Patrick J Halvey, Jason M Hansen, Matt Reed, Jan Pohl, Dean P Jones

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

53 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Acute Hyperglycemia Exacerbates Hemorrhagic Transformation after Embolic Stroke and Reperfusion with tPA: A Possible Role of TXNIP-NLRP3 Inflammasome.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2022
    Article
  6. Review
  7. Article
  8. Protein Lipoxidation: Basic Concepts and Emerging Roles.Antioxidants (Basel, Switzerland) · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Hesperetin mitigates acrolein-induced apoptosis in lung cells in vitro and in vivo.Redox report : communications in free radical research · 2018
    Article
  13. Review
  14. Review
  15. Review
  16. Redox theory of aging: implications for health and disease.Clinical science (London, England : 1979) · 2017
    Review
  17. Oxidative medicine and cellular longevity · 2017
    Article
  18. Review
  19. Article
  20. The role of oxysterols in vascular ageing.The Journal of physiology · 2016
    Review
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

6 authors at 1 institution in 1 country.

Young-Mi GoDepartment of Medicine (Division of Pulmonary Medicine), Emory University, Atlanta, GA 30322, USA.
Patrick J Halvey
Jason M Hansen
Matt Reed
Jan Pohl
Dean P Jones
Emory University · US

Funding

Thioredoxin-2 protection against mitochondrial oxidative toxicityR01ES009047 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 1998 to 2013
$3.9M
Nuclear and Cytoplasmic Redox in Oxidative StressR01ES011195 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2001 to 2011
$3.3M
NIEHS NIH HHS ES011195NIEHS NIH HHS ES09047NIEHS NIH HHS R01 ES009047NIEHS NIH HHS R01 ES011195
6 · The paper itself

Abstract

Several lines of evidence suggest that an increase in aldehyde-modified proteins is associated with development of atherosclerosis. Acrolein and 4-hydroxynonenal (HNE) are reactive aldehydes generated during active inflammation as a consequence of lipid peroxidation; both react with protein thiols, including thioredoxin-1 (Trx1), a protein recently found to regulate antioxidant function in endothelial cells. The present study examined whether acrolein or HNE modification of Trx1 could potentiate monocyte adhesion to endothelial cells, an early event of atherosclerosis. We examined the function of acrolein and HNE-modified Trx1 in the regulation of the early events of atherosclerosis using cultured aortic endothelial cells as a vascular model system, for in vitro enzymatic assay, and in mass spectrometry analysis. Our data show that acrolein and HNE at 1:1 ratios with Trx1 modified Cys-73 and inhibited activity. In endothelial cells, adducts were detected at concentrations as low as 1 mumol/L including conditions in which there was no detectable change in glutathione. Acrolein and HNE modification of Trx1 was associated with increased production of reactive oxygen species. Microinjection of acrolein- and HNE-modified Trx1 into endothelial cells stimulated monocyte adhesion. Chemical modification of Trx1 by common environmental and endogenously generated reactive aldehydes can contribute to atherosclerosis development by interfering with antioxidant and redox signaling functions of Trx1.

Indexed as

AcroleinAldehydesAmino Acid SequenceAnimalsAortaAtherosclerosisCattleCell AdhesionCell LineEndothelial CellsGlutathioneHumansInflammationJNK Mitogen-Activated Protein KinasesMolecular Sequence DataMonocytes4-hydroxy-2-nonenalAcroleinAldehydesGlutathioneJNK Mitogen-Activated Protein KinasesNF-kappa BReactive Oxygen SpeciesThioredoxinsTXN protein, human

Identifiers

PMID17982132
PMCPMC2043527
OpenAlexW2017058712

What OpenQuestion holds

Textmetadata
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.