Evidence map›Paper›PMID 34017341›Full record

ArticleFrontiers in immunology2021

An Integrative Transcriptomic and Metabolomic Study Revealed That Melatonin Plays a Protective Role in Chronic Lung Inflammation by Reducing Necroptosis.

Kaimin Mao, Ping Luo, Wei Geng, Juanjuan Xu, Yuhan Liao, Hua Zhong, Pei Ma, Qi Tan, Hui Xia, Limin Duan and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  19. Role of melatonin in respiratory diseases (Review).Experimental and therapeutic medicine · 2022
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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

16 authors at 5 institutions in 1 country.

Kaimin MaoDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ping LuoCenter for Translational Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wei GengDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Juanjuan XuDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yuhan LiaoDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hua ZhongCollege of Life Sciences, Wuhan University, Wuhan, China.
Pei MaDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Qi TanDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui XiaDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Limin DuanDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Siwei SongDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Danling LongDepartment of Stomatology, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Yuqi LiuDepartment of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Tinglin YangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yali WuDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yang JinDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of the National Health Commission Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNUnion Hospital · CNHubei University of Medicine · CNUnion Hospital · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported that melatonin can relieve the symptoms of chronic obstructive pulmonary disease (COPD) by improving sleep quality, that is to say, the pineal secreted hormone melatonin has a protective effect in the pathogenesis of COPD, but its underlying mechanism remains unclear. In this study, we recruited 73 people into control (n = 22), stable COPD (n = 20), and acute exacerbation of COPD (n = 31) groups to detect the serum melatonin levels. Then, through the mouse model, we employed a systematic study based on the metabolomic and transcriptomic analyses to investigate the molecular mechanisms involved in the progression of the disease. Circulating melatonin in acute exacerbation of COPD patients was decreased compared with that in healthy donors and stable COPD patients. The serum melatonin level was positively correlated with lung function parameters, such as FEV1, FEV1/FVC, and FEV1% predicted in acute exacerbation of COPD patients. Animal experiments showed that melatonin can not only alleviate chronic lipopolysaccharide (LPS)-induced mouse lung destruction and chronic lung inflammation but also reduce necroptosis (RIP1/RIP3/MLKL), a programmed cell death process in bronchial epithelial cells. The protective effect of melatonin on chronic lung inflammation was further suggested to be dependent on targeting its membrane receptor MT1/MT2. In addition, transcriptomic and metabolomic profiling in the lungs of mice indicated that LPS can induce perturbations of the mainstream metabolites associated with amino acid and energy metabolism. Melatonin may reduce the necroptosis by modifying the disordered pathways of alanine, aspartate, and glutamate metabolism caused by LPS. This study suggests that melatonin may act as a potential therapeutic agent for alleviating the chronic inflammation associated with COPD.

Indexed as

MetabolomeNecroptosisTranscriptomeAnimalsBiomarkersCase-Control StudiesDisease Models, AnimalDisease ProgressionFemaleGene Expression ProfilingHumansLungMaleMelatoninMetabolomicsMiceBiomarkersMelatoninchronic lung inflammationCOPDmelatoninmetabolomicnecroptosistranscriptomic

Identifiers

PMID34017341
PMCPMC8129533
OpenAlexW3159010180

What Socratic holds

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LicenceCC BY
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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 Socratic graph.