Evidence map›Paper›PMID 39625494›Full record

ArticleLung2024

The Mitochondrial Fusion Promoter M1 Mitigates Cigarette Smoke-Induced Airway Inflammation and Oxidative Stress via the PI3K-AKT Signaling Pathway.

Tingting Zeng, Lian Liu, Dan Xu, Tao Wang, Yanqiu Wu, Jiangyue Qin, Lijuan Gao, Mei Chen, Xiaohua Li, Diandian Li and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Tingting Zeng *State Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Lian Liu *State Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Dan XuState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Tao WangState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Yanqiu WuState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Jiangyue QinState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Lijuan GaoState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Mei ChenSchool of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Xiaohua LiDepartment of Respiratory and Critical Care Medicine, Sixth People's Hospital of Chengdu, Chengdu, 610051, China.
Diandian LiState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Jun ChenState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China. junchen@scu.edu.cn.
Yongchun ShenState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China. shen_yongchun@126.com.
Fuqiang WenState Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.

Funding

the 1⋅3⋅5 project for disciplines of excellence, West China Hospital, Sichuan University ZYGD23009the China Posdoctoral Science Foundation 2021M702350the National Natural Science Foundation of China 82170046, 31871157, 82100047, and 82300050the Sichuan Key Research and Development Program 2024NSFSC1522, 2022YFS0104
6 · The paper itself

Abstract

purposeThis study investigated the efficacy and underlying mechanism of the mitochondrial fusion promoter M1 in mitigating cigarette smoking (CS)-induced airway inflammation and oxidative stress both in vitro and in vivo models.

methodsCigarette smoke extract (CSE)-treated airway epithelial cells (BEAS-2B) and CS-exposed mice were pretreated with M1, followed by the measurement of proinflammatory cytokines, oxidative stress, mitochondrial fusion proteins (MFN2 and OPA1) and fission proteins (DRP1 and MFF). Molecular pathways were elucidated through transcriptomic analysis and Western blotting.

resultsM1 pretreatment in CSE-treated cells significantly reduced the release of inflammatory cytokines (interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF)-α); reduced malondialdehyde (MDA) and reactive oxygen species (ROS) levels; increased superoxide dismutase (SOD) activity; protected mitochondrial function by increasing the expression of mitochondrial fusion proteins (MFN2 and OPA1) and decreasing the expression of mitochondrial fission proteins (DRP1 and MFF). M1 attenuated CS-induced lung histologic damage and mucus hypersecretion in mice, relieved high oxidative stress and reduced the release of IL-6 and IL-8 in BALF. Similarly, it also protected mitochondrial function by regulating the CS-induced imbalance of mitochondrial dynamic proteins. Transcriptome sequencing and Western blotting showed that M1 inhibited CSE- or CS-induced activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT) signaling pathway.

conclusionM1 plays a protective role in inflammation, oxidative stress and mitochondrial dynamics dysfunction caused by CS by inhibiting the PI3K-AKT signaling pathway; thus, it has therapeutic potential for the treatment of CS-induced airway disorders.

Indexed as

Mitochondrial DynamicsOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsCell LineCigarette SmokingCytokinesDisease Models, AnimalEpithelial CellsHumansLungMaleMiceMice, Inbred C57BLCytokinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSmokeAirway inflammationChronic obstructive pulmonary diseaseMitochondrial fusion promoter M1Oxidative stress

Identifiers

PMID39625494

What OpenQuestion holds

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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.