Air-Liquid Interface (ALI) Exposure of Human Bronchial Epithelial Cells to Whole Gasoline Engine Exhaust Disrupts Autophagy and Proinflammatory Responses.

Guoliang Li, Tao Yu, Xueyan Zhang, Wei Zhao, Min Zheng, Ying Qu, Bin Li, Ping Bin

Abstract read

In one paragraph

Article in Toxics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Guoliang LiNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Tao YuNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Xueyan ZhangNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Wei ZhaoNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Min ZhengNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Ying QuNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

Bin LiNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.ORCID 0000-0003-4002-5723

Ping BinNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.ORCID 0000-0002-2659-2396

Funding

National Natural Science Foundation of China 82073596 and 81472955

6 · The paper itself

Abstract

Gasoline engine exhaust (GEE) has been reported to contribute to the pathogenesis of pulmonary diseases. Autophagy, proinflammatory cytokines, and the NF-κB pathway core protein may play roles in the development of lung diseases caused by GEE. However, little is known about the possible toxic effects. Herein, we aimed to examine the crosstalk between GEE and the expression levels of autophagy-associated proteins (microtubule-associated proteins 1A/1B light chain 3A (LC3I/II)), proinflammatory cytokine genes (including

Indexed as

air-liquid interface exposureautophagygasoline engine exhausthuman epithelial cellsNF-κB pathwayproinflammatory cytokines

Identifiers

PMID41893457

DOI10.3390/toxics14030188

PMCPMC13029995

What OpenQuestion holds

Textmetadata

LicenceCC BY

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Registered trials

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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.