Evidence map›Paper›PMID 41376971›Full record

ArticleJournal of thoracic disease2025

Involvement of mitochondrial unfolded protein response and activating transcription factor 4 in the mitochondrial damage pathway of BEAS-2B cells induced by cigarette smoke extracts.

Jie Jin, Tiantian Cen, Minxuan Huang, Feng Xu, Qunli Ding, Dan Lv, Shanshan Wang, Lin Fei, Hongying Ma, Panfeng Fu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Mulberroside A attenuates HMolecular medicine reports · 2026
    Article
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

10 authors.

Jie Jin *Department of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Tiantian Cen *Department of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Minxuan HuangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Feng XuCentral Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Qunli DingDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Dan LvDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Shanshan WangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Lin FeiDepartment of Respiratory and Critical Care Medicine, The People's Hospital of Cixi City, Cixi, China.
Hongying MaDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Panfeng FuDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University, Ningbo, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cigarette smoke extract (CSE) induces reactive oxygen species (ROS) generation in human bronchial epithelial cells, leading to mitochondrial dysfunction and subsequently triggering the mitochondrial unfolded protein response (UPR Methods: BEAS-2B bronchial epithelial cells were treated with different concentrations of CSE, and mitochondrial function was detected by JC-1 staining and MitoSoxRed staining. The expression and localisation of translocase of inner mitochondrial membrane 23 (Tim23) and ATF-4 were detected by Western blot method and immunofluorescence staining with laser confocal microscopy. Results: The study showed decreased membrane potential and mitochondrial ROS accumulation in BEAS-2B cells after CSE treatment, which indicated that CSE caused mitochondrial dysfunction and oxidative stress. The expression of Tim23 was up-regulated after CSE exposure; this alteration hints at a potential activation of mitochondrial stress pathways. The expression of ATF-4 showed a positive correlation with the time of CSE treatment, and the expression in the nucleus was increased, which indicated that CSE altered the expression and localisation of Tim23 and ATF-4. Conclusions: CSE leads to a decrease in mitochondrial membrane potential and an increase in ROS generation, and triggers alterations in the expression of Tim23 and ATF-4. These findings are consistent with the model that CSE may impair mitochondrial homeostasis, potentially through mechanisms involving mitochondrial stress responses (such as UPR

Indexed as

activating transcription factor 4 (ATF-4)BEAS-2BCigarette smoke extract (CSE)mitochondrial unfolded protein response (UPRmt)

Identifiers

PMID41376971
PMCPMC12688523

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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.