Evidence map›Paper›PMID 28115642›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2017

Omega-3 Polyunsaturated Fatty Acids Protect Against Cigarette Smoke-Induced Oxidative Stress and Vascular Dysfunction.

Elani F Wiest, Mary T Walsh-Wilcox, Mary K Walker

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. A Review ofNutrients · 2019
    Pooled it
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  5. Article
  6. Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
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  20. EXCLI journal · 2019
    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

3 authors at 1 institution in 1 country.

Elani F WiestDepartment of Pharmaceutical Sciences, University of New Mexico, Albuquerque, New Mexico 87131.
Mary T Walsh-WilcoxDepartment of Pharmaceutical Sciences, University of New Mexico, Albuquerque, New Mexico 87131.
Mary K WalkerDepartment of Pharmaceutical Sciences, University of New Mexico, Albuquerque, New Mexico 87131.
University of New Mexico · US

Funding

Vasoprotective mechanisms of n-3 PUFA epoxidesR15HL130970 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI WALKER, MARY K · 2016 to 2016
$455k
Human CYP1A1, diet and dioxin-induced hypertensionR15ES021896 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI WALKER, MARY K · 2012 to 2012
$453k
NHLBI NIH HHS R15 HL130970NIEHS NIH HHS R15 ES021896
6 · The paper itself

Abstract

In cigarette smokers endothelial dysfunction, measured by flow-mediated dilation (FMD), precedes cardiovascular disease (CVD) and can be improved by supplementation with n - 3 polyunsaturated fatty acids (PUFAs). We developed a mouse model of cigarette smoke (CS)-induced endothelial dysfunction that resembles impaired FMD observed in human cigarette smokers and investigated the mechanism by which n - 3 PUFAs mediate vasoprotection. We hypothesized that loss of nitric oxide (NO)-dependent vasodilation in CS-exposed mice would be prevented by dietary n - 3 PUFAs via a decrease in oxidative stress. C57BL/6 mice were fed a chow or n - 3 PUFA diet for 8 weeks and then exposed to mainstream CS or filtered air for 5 days, 2 h/day. Mesenteric arterioles were preconstricted with U46619 and dilated by stepwise increases in pressure (0-40 mmHg), resulting in increases in flow, ± inhibitor of NO production or antioxidant, Tempol. Markers of oxidative stress were measured in lung and heart. CS-exposed mice on a chow diet had impaired FMD, resulting from loss of NO-dependent dilation, compared with air exposed mice. Tempol restored FMD by normalizing NO-dependent dilation and increasing NO-independent dilation. CS-exposed mice on the n - 3 PUFA diet had normal FMD, resulting from a significant increase in NO-independent dilation, compared with CS-exposed mice on a chow diet. Furthermore, n - 3 PUFAs decreased two CS-induced markers of oxidative stress, 8-epiprostaglandin-F2α levels and heme oxygenase-1 mRNA, and significantly attenuated CS-induced cytochrome P4501A1 mRNA expression. These data demonstrate that dietary n - 3 PUFAs can protect against CS-induced vascular dysfunction via multiple mechanisms, including increasing NO-independent vasodilation and decreasing oxidative stress.

Indexed as

Dietary SupplementsOxidative StressAnimalsAntioxidantsArteriolesAtmosphere Exposure ChambersBiomarkersCardiovascular AgentsCigarette SmokingEndothelium, VascularFatty Acids, Omega-3Gene Expression Regulation, EnzymologicHeart VentriclesLungMaleMesenteric ArteriesAntioxidantsBiomarkersCardiovascular AgentsFatty Acids, Omega-3Smokecigarette smokeflow-mediated dilationomega-3 polyunsaturated fatty acidsoxidative stressvasodilation.

Identifiers

PMID28115642
PMCPMC6075584
OpenAlexW2581417117

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.