Evidence map›Paper›PMID 19270193›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Glutathione-S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke.

Daniel J Conklin, Petra Haberzettl, Russell A Prough, Aruni Bhatnagar

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 108 citations in OpenAlex.

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  18. Peroxiredoxin6 in Endothelial Signaling.Antioxidants (Basel, Switzerland) · 2019
    Review
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  20. Article

3 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Daniel J ConklinInstitute of Molecular Cardiology, Div. of Cardiovascular Medicine, Dept. of Medicine, Univ. of Louisville, Delia Baxter Bldg., 580 S. Preston St., Rm. 421C, Louisville, KY 40202, USA. dj.conklin@louisville.edu
Petra Haberzettl
Russell A Prough
Aruni Bhatnagar
University of Louisville · US

Funding

Role of Platelet Activation and Vascular Pathology in Aldehyde ToxicityP01ES011860 · NIEHS · UNIVERSITY OF LOUISVILLE · PI PIERCE, WILLIAM M · 2003 to 2007
$7.0M
Cardioprotective Mechanisms of Glutathione S-transferase PR01HL089380 · NHLBI · UNIVERSITY OF LOUISVILLE · PI CONKLIN, DANIEL JOSEPH · 2008 to 2012
$2.1M
NHLBI NIH HHS HL-89380NHLBI NIH HHS R01 HL089380NIEHS NIH HHS ES-11860
6 · The paper itself

Abstract

Exposure to tobacco smoke impairs endothelium-dependent arterial dilation. Reactive constituents of cigarette smoke are metabolized and detoxified by glutathione-S-transferases (GSTs). Although polymorphisms in GST genes are associated with the risk of cancer in smokers, the role of these enzymes in regulating the cardiovascular effects of smoking has not been studied. The P isoform of GST (GSTP), which catalyzes the conjugation of electrophilic molecules in cigarette smoke such as acrolein, was expressed in high abundance in the mouse lung and aorta. Exposure to tobacco smoke for 3 days (5 h/day) decreased total plasma protein. These changes were exaggerated in GSTP(-/-) mice. Aortic rings isolated from tobacco smoke-exposed GSTP(-/-) mice showed greater attenuation of ACh-evoked relaxation than those from GSTP(+/+) mice. The lung, plasma, and aorta of mice exposed to tobacco smoke or acrolein (for 5 h) accumulated more acrolein-adducted proteins than those tissues of mice exposed to air, indicating that exposure to tobacco smoke results in the systemic delivery of acrolein. Relative to GSTP(+/+) mice, modification of some proteins by acrolein was increased in the aorta of GSTP(-/-) mice. Aortic rings prepared from GSTP(-/-) mice that inhaled acrolein (1 ppm, 5 h/day for 3 days) or those exposed to acrolein in an organ bath showed diminished ACh-induced arterial relaxation more strongly than GSTP(+/+) mice. Acrolein-induced endothelial dysfunction was prevented by pretreatment of the aorta with N-acetylcysteine. These results indicate that GSTP protects against the endothelial dysfunction induced by tobacco smoke exposure and that this protection may be related to the detoxification of acrolein or other related cigarette smoke constituents.

Indexed as

AcetylcholineAcetylcysteineAcroleinAnimalsAntioxidantsAorta, ThoracicBlood ProteinsDose-Response Relationship, DrugEndothelium, VascularGlutathione S-Transferase piInhalation ExposureLungMaleMiceMice, KnockoutNicotianaAcetylcholineAcetylcysteineAcroleinAntioxidantsBlood ProteinsGlutathione S-Transferase piGstp1 protein, mouseNitroprussideSmokeVasodilator Agents

Identifiers

PMID19270193
PMCPMC2685347
OpenAlexW1993516648

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.