Evidence map›Paper›PMID 40598160›Full record

ArticleBMC medicine2025

Disability in mitochondrial aerobic metabolism and Mg

Ze Zhang, Gan Miao, Juan Ma, Ziyuan Li, Chuer Zheng, Jian Ding, Hao Yin, Xiangcheng Cui, Shoujie Dai, Rifat Zubair Ahmed and 4 more

Abstract read
In one paragraph

Article in BMC medicine, 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. 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

14 authors.

Ze Zhang *Department of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Gan Miao *Department of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Juan MaState Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
Ziyuan LiDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Chuer ZhengDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Jian DingDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Hao YinDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China.
Xiangcheng CuiPingdu Municipal Centers for Diseases Control and Prevention, Qingdao, China.
Shoujie DaiPingdu Municipal Centers for Diseases Control and Prevention, Qingdao, China.
Rifat Zubair AhmedDepartment of Genetics, University of Karachi, Karachi, Pakistan.
Yong NiuKey Laboratory of Chemical Safety and Health, Chinese Center for Disease Control and Prevention, National Institute for Occupational Health and Poison Control, Beijing, China.
Shanfa YuDepartment of Public Health, Henan Medical College, Zhengzhou, China.
Xiaoting JinDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China. xtjin@qdu.edu.cn.
Yuxin ZhengDepartment of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao, China. yxzheng@qdu.edu.cn.

Funding

National Natural Science Foundation of China 82241086National Natural Science Foundation of China 82473609National Natural Science Foundation of China 82473674Taishan Scholars Program of Shandong Province tsqn201909101
6 · The paper itself

Abstract

backgroundIschemic heart disease (IHD) is a major cardiovascular health concern. In addition to metabolic and behavioral risks, diesel particulate matter (DPM), with a widely exposed population, is an important external environmental risk factor for IHD. However, the effect biomarkers used to diagnose DPM-caused IHD and underlying mechanisms remain unknown. We investigated the biomarkers and underlying mechanisms of DPM in relation to myocardial hypoxia injury.

methodsThis study applied a unique population of diesel engine testers with stable DPM exposure. Electrocardiogram examination, echocardiogram examination, serum levels of myocardial enzymes, and 6-min walking test were used for the myocardial risks assessment. A mouse model exposed to occupational environmental DPM dose and in vitro models of DPM-induced myocardial hypoxia injury were used for assessment of mitochondrial aerobic metabolism via the oxygraph-2k system, western blotting, and kits. Ion fluorescence probes, ion supplements, and mitochondrial RNA splicing protein 2 (Mrs2) overexpression transfection were used in further investigations and verifications of the mechanism of mitochondrial Mg

resultsWe identified compromised myocardial mitochondrial aerobic metabolism as a precursor biomarker for the cardiac risk of myocardial hypertrophy and hypoxia injury in DPM exposure. DPM induce mitochondrial Mg

conclusionsOur findings show that compromised mitochondrial aerobic metabolism, associated with Mg

Indexed as

MagnesiumMitochondriaMitochondria, HeartMyocardial IschemiaParticulate MatterVehicle EmissionsAnimalsBiomarkersHumansMaleMiceMice, Inbred C57BLBiomarkersMagnesiumParticulate MatterVehicle EmissionsDiesel particulate matterIschemic heart diseaseMg2+ transportMitochondrial aerobic metabolism

Identifiers

PMID40598160
PMCPMC12218838

What OpenQuestion holds

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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.