Evidence map›Paper›PMID 33237957›Full record

ArticlePloS one2020

Heat-Not-Burn cigarette induces oxidative stress response in primary rat alveolar epithelial cells.

Yoko Ito, Kana Oshinden, Naokata Kutsuzawa, Chinatsu Kohno, Sanae Isaki, Keiko Yokoyama, Tadayuki Sato, Masayuki Tanaka, Koichiro Asano

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Yoko ItoDivision of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.ORCID 0000-0002-7791-1967
Kana OshindenDivision of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Naokata KutsuzawaDivision of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Chinatsu KohnoDivision of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Sanae IsakiDepartment of Bioinformatics and Molecular Biology, Support Center for Medical Research and Education, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Keiko YokoyamaDepartment of Bioinformatics and Molecular Biology, Support Center for Medical Research and Education, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Tadayuki SatoDepartment of Bioinformatics and Molecular Biology, Support Center for Medical Research and Education, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Masayuki TanakaDepartment of Bioinformatics and Molecular Biology, Support Center for Medical Research and Education, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Koichiro AsanoDivision of Pulmonary Medicine, Department of Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There has been an increase in the usage of heat-not-burn (HNB) cigarette products. However, their effects on alveolar epithelial cells (AECs) remain unknown. AECs are the target cells of conventional cigarette smoking-related respiratory diseases such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and lung cancer whose pathogenesis involves oxidative stress. In this study, primary rat AECs were isolated, cultured and stimulated by HNB cigarette smoke extract (CSE). Our data indicate that rat AECs exposed to HNB CSE induced oxidative stress response genes (e.g. Hmox-1, Gsta1, Gsta3 and Nqo1). We also compared the oxidative stress response between two different types of AECs, alveolar type I-like (ATI-like) cells and type II (ATII) cells, and between two different types of cigarette, HNB cigarettes and conventional cigarettes. The expressions of Gsta1, Gsta3 and Nqo1 were higher in ATII cells than ATI-like cells in response to HNB and conventional cigarettes, but there was no significant difference in their expression levels between HNB cigarette and conventional cigarette. Taken together, our results suggest that HNB cigarettes have the similar potential as conventional cigarette products to induce oxidative stress response in AECs.

Indexed as

Alveolar Epithelial CellsAnimalsCigarette SmokingDisease Models, AnimalElectronic Nicotine Delivery SystemsHot TemperatureHumansNicotianaOxidation-ReductionOxidative StressPrimary Cell CulturePulmonary AlveoliPulmonary Disease, Chronic ObstructiveRatsSmokeSmoke

Identifiers

PMID33237957
PMCPMC7688177
OpenAlexW3107245017

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.