Evidence map›Paper›PMID 29078374›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Taurine ameliorates particulate matter-induced emphysema by switching on mitochondrial NADH dehydrogenase genes.

Xiaobo Li, Hongbao Yang, Hao Sun, Runze Lu, Chengcheng Zhang, Na Gao, Qingtao Meng, Shenshen Wu, Susanna Wang, Michael Aschner and 5 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 75 citations in OpenAlex.

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  16. Particulate matter in COPD pathogenesis: an overview.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 2 countries.

Xiaobo LiKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Hongbao YangCenter for New Drug Safety Evaluation and Research, China Pharmaceutical University, Nanjing 211198, China.
Hao SunKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Runze LuKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Chengcheng ZhangKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Na GaoKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Qingtao MengKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Shenshen WuKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
Susanna WangDepartment of Neurology, University of Southern California, Los Angeles, CA 90089.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461.
Jiong WuDepartment of Life Science, Zhejiang Technology University, Hangzhou 310018, China.
Boping TangJiangsu Key Laboratory for Bioresources of Saline Soils, Jiangsu Synthetic Innovation Center for Coastal Bioagriculture, Yancheng Teachers University, Yancheng 224002, China.
Aihua GuState Key Laboratory of Reproductive Medicine, Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 211166, China.
Steve A KayDepartment of Neurology, University of Southern California, Los Angeles, CA 90089; stevekay@usc.edu rui.chen@seu.edu.cn.ORCID 0000-0002-0402-2878
Rui ChenKey Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China; stevekay@usc.edu rui.chen@seu.edu.cn.
Southeast University · CNUniversity of Southern California · USAlbert Einstein College of Medicine · USChina Pharmaceutical University · CNNanjing Medical University · CNYancheng Teachers University · CN

Funding

Mechanisms of Manganese NeurotoxicityR01ES010563 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 2001 to 2026
$11.9M
Mechanisms of Methylmercury Induced Neuron ToxicityR01ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 1996 to 2026
$10.6M
Genetic Modulation of MeHg-Induced Oxidative Stress in the Developing BrainR01ES020852 · NIEHS · VANDERBILT UNIVERSITY · PI ASCHNER, MICHAEL · 2012 to 2016
$1.8M
NIEHS NIH HHS R01 ES007331NIEHS NIH HHS R01 ES010563NIEHS NIH HHS R01 ES020852
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) has been linked to particulate matter (PM) exposure. Using transcriptomic analysis, we demonstrate that diesel exhaust particles, one of the major sources of particulate emission, down-regulated genes located in mitochondrial complexes I and V and induced experimental COPD in a mouse model. 1-Nitropyrene was identified as a major toxic component of PM-induced COPD. In the panel study, COPD patients were found to be more susceptible to PM than individuals with normal lung function due to an increased inflammatory response. Mechanistically, exposure to PM in human bronchial epithelial cells led to a decline in CCAAT/enhancer-binding protein alpha (C/EBPα), which triggered aberrant expression of NADH dehydrogenase genes and ultimately led to enhanced autophagy. ATG7-deficient mice, which have lower autophagy rates, were protected from PM-induced experimental COPD. Using metabolomics analysis, we further established that treatment with taurine and 3-methyladenine completely restored mitochondrial gene expression levels, thereby ameliorating the PM-induced emphysema. Our studies suggest a potential therapeutic intervention for the C/EBPα/mitochondria/autophagy axis in PM-induced COPD.

Indexed as

AdenineAgedAnimalsAutophagyCCAAT-Enhancer-Binding ProteinsCell LineEpithelial CellsFemaleGenes, MitochondrialHumansLungMaleMiceMice, Inbred C57BLMiddle AgedMitochondria3-methyladenineAdenineCCAAT-Enhancer-Binding ProteinsNADH DehydrogenaseParticulate MatterTaurineautophagychronic obstructive pulmonary diseasemitochondriaparticulate mattertaurine

Identifiers

PMID29078374
PMCPMC5692577
OpenAlexW2765500098

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.