Evidence map›Paper›PMID 26582801›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2016

Effects of Cigarette Smoke, Cessation, and Switching to Two Heat-Not-Burn Tobacco Products on Lung Lipid Metabolism in C57BL/6 and Apoe-/- Mice-An Integrative Systems Toxicology Analysis.

Bjoern Titz, Stéphanie Boué, Blaine Phillips, Marja Talikka, Terhi Vihervaara, Thomas Schneider, Catherine Nury, Ashraf Elamin, Emmanuel Guedj, Michael J Peck and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  12. Ambient PMEnvironment international · 2021
    Article
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  19. Article
  20. Lipid metabolism in chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 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

22 authors at 2 institutions in 3 countries.

Bjoern Titz*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland; *Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland; julia.hoeng@pmi.com.
Stéphanie Boué*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Blaine PhillipsPhilip Morris International Research Laboratories, 50 Science Park Road, Singapore, Singapore; and.
Marja Talikka*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Terhi VihervaaraZora Biosciences Oy, Biologinkuja 1, 02150 Espoo, Finland.
Thomas Schneider*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Catherine Nury*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Ashraf Elamin*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Emmanuel Guedj*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Michael J Peck*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Walter K Schlage*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Maciej Cabanski*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Patrice Leroy*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Gregory Vuillaume*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Florian Martin*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Nikolai V Ivanov*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Emilija Veljkovic*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Kim EkroosZora Biosciences Oy, Biologinkuja 1, 02150 Espoo, Finland.
Reijo LaaksonenZora Biosciences Oy, Biologinkuja 1, 02150 Espoo, Finland.
Patrick Vanscheeuwijck*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Manuel C Peitsch*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland;
Julia Hoeng*Philip Morris International Research and Development, Quai Jeanrenaud 5, 2000 Neuchatel, Switzerland; julia.hoeng@pmi.com.
Philip Morris International (Switzerland) · CHZora Biosciences (Finland) · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The impact of cigarette smoke (CS), a major cause of lung diseases, on the composition and metabolism of lung lipids is incompletely understood. Here, we integrated quantitative lipidomics and proteomics to investigate exposure effects on lung lipid metabolism in a C57BL/6 and an Apolipoprotein E-deficient (Apoe(-/-)) mouse study. In these studies, mice were exposed to high concentrations of 3R4F reference CS, aerosol from potential modified risk tobacco products (MRTPs) or filtered air (Sham) for up to 8 months. The 2 assessed MRTPs, the prototypical MRTP for C57BL/6 mice and the Tobacco Heating System 2.2 for Apoe(-/-) mice, utilize "heat-not-burn" technologies and were each matched in nicotine concentrations to the 3R4F CS. After 2 months of CS exposure, some groups were either switched to the MRTP or underwent cessation. In both mouse strains, CS strongly affected several categories of lung lipids and lipid-related proteins. Candidate surfactant lipids, surfactant proteins, and surfactant metabolizing proteins were increased. Inflammatory eicosanoids, their metabolic enzymes, and several ceramide classes were elevated. Overall, CS induced a coordinated lipid response controlled by transcription regulators such as SREBP proteins and supported by other metabolic adaptations. In contrast, most of these changes were absent in the mice exposed to the potential MRTPs, in the cessation group, and the switching group. Our findings demonstrate the complex biological response of the lungs to CS exposure and support the benefits of cessation or switching to a heat-not-burn product using a design such as those employed in this study.

Indexed as

Lipid MetabolismAnimalsApolipoproteins EEicosanoidsFemaleLungMiceMice, Inbred C57BLOxidative StressProteomeSmokeSphingolipidsTobacco ProductsApolipoproteins EEicosanoidsProteomeSmokeSphingolipidslipidomicsmodified risk tobacco productsquantitative proteomicssystems toxicology

Identifiers

PMID26582801
PMCPMC4725611
OpenAlexW2187782573

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.