Evidence map›Paper›PMID 28808421›Full record

ArticleInternational journal of biological sciences2017

Crosstalk between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells.

Guangju Zhao, Kaiqiang Cao, Changqin Xu, Aifang Sun, Wang Lu, Yi Zheng, Haixiao Li, Guangliang Hong, Bing Wu, Qiaomeng Qiu and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 64 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

11 authors at 2 institutions in 1 country.

Guangju ZhaoEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Kaiqiang CaoEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Changqin XuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Aifang SunEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Wang LuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Yi ZhengDepartment of Microbiology and immunology, School of Laboratory Medicine, Wenzhou Medical University, Wenzhou 325000, China.
Haixiao LiEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Guangliang HongEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Bing WuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Qiaomeng QiuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Zhongqiu LuEmergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
First Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paraquat (PQ), as a highly effective and nonselective herbicide, induces cell apoptosis through generation of superoxide anions which forms reactive oxygen species (ROS). Mitochondria, as regulators for cellular redox signaling, have been proved to play an important role in PQ-induced cell apoptosis. This study aimed to evaluate whether and how mitochondrial fission interacts with oxidative stress in PQ-induced apoptosis in mouse alveolar type II (AT-II) cells. Firstly, we demonstrated that PQ promoted apoptosis and release of cytochrome-c (Cyt-c). Furthermore, we showed that PQ broke down mitochondrial network, enhanced the expression of fission-related proteins, increased Drp1 mitochondrial translocation while decreased the expression of fusion-related proteins in AT-II cells. Besides, inhibiting mitochondrial fission using mdivi-1, a selective inhibitor of Drp1, markedly attenuated PQ-induced apoptosis, release of Cyt-c and the generation of ROS. These results indicate that mitochondrial fission involves in PQ-induced apoptosis. Further study demonstrated that antioxidant ascorbic acid inhibited Drp1 mitochondrial translocation, mitochondrial fission and attenuated PQ-induced apoptosis. Overall, our findings suggest that mitochondrial fission interplays with ROS in PQ-induced apoptosis in mouse AT-II cells and mitochondrial fission could serve as a potential therapeutic target in PQ poisoning.

Indexed as

Alveolar Epithelial CellsAnimalsApoptosisAscorbic AcidCells, CulturedCell SurvivalCytochromes cDeath-Associated Protein KinasesHerbicidesMiceMitochondrial DynamicsOxidative StressParaquatProtein TransportAscorbic AcidCytochromes cDeath-Associated Protein KinasesHerbicidesParaquatapoptosismitochondrial fissionoxidative stressparaquatreactive oxygen species.

Identifiers

PMID28808421
PMCPMC5555106
OpenAlexW2739538295

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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.