Evidence map›Paper›PMID 34419168›Full record

ArticleClinical epigenetics2021

DNA methylome profiling reveals epigenetic regulation of lipoprotein-associated phospholipase A

Jingjin Li, Xiaoping Zhang, Mengxi Yang, Hang Yang, Ning Xu, Xueqiang Fan, Gang Liu, Xintong Jiang, Jiasai Fan, Lifang Zhang and 9 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  10. Vulnerable Atherosclerotic Plaque: Is There a Molecular Signature?International journal of molecular sciences · 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

19 authors at 5 institutions in 2 countries.

Jingjin Li *Department of Cardiology, Beijing Tiantan Hospital of Capital Medical University, Beijing, China.
Xiaoping Zhang *Beijing Anzhen Hospital of Capital Medical University and Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China.
Mengxi Yang *Department of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Hang YangState Key Laboratory for Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Ning XuDepartment of Medicine, Karolinska Institute, Stockholm, Sweden.
Xueqiang FanDepartment of Cardiovascular Surgery, China-Japan Friendship Hospital, Beijing, China.
Gang LiuDepartment of Cardiovascular Surgery, Peking University People's Hospital, Beijing, China.
Xintong JiangDepartment of Rheumatology and Immunology, Peking University People's Hospital, Beijing, China.
Jiasai FanDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Lifang ZhangDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Hu ZhangDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Ying ZhouDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Rui LiDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Si GaoDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Jiangli JinDepartment of Neurology, China-Japan Friendship Hospital, Beijing, China.
Zening JinDepartment of Cardiology, Beijing Tiantan Hospital of Capital Medical University, Beijing, China.
Jingang ZhengDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Qiang TuState Key Laboratory for Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Jingyi RenDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China. renjingyi1213@hotmail.com.ORCID 0000-0002-9424-4713
China-Japan Friendship Hospital · CNCapital Medical University · CNPeking University · CNChinese Academy of Sciences · CNKarolinska Institutet · SE

Funding

Beijing Health Technologies Promotion Program BHTPP202004National Natural Science Foundation of China 81270276National Natural Science Foundation of China 81500365National Natural Science Foundation of China 81770359Natural Science Foundation of Beijing Municipality 7172040Open Project Fund of State Key Laboratory of Molecular Developmental Biology of China 2020-MDB-KF-17Open Project Fund of State Key Laboratory of Molecular Developmental Biology of China 2021-MDB-KF-18
6 · The paper itself

Abstract

backgroundAtherosclerotic plaque vulnerability is a key feature of atheroprogression and precipitating acute cardiovascular events. Although the pivotal role of epigenetic regulation in atherosclerotic plaque destabilization is being recognized, the DNA methylation profile and its potential role in driving the progression and destabilization of atherosclerotic cardiovascular disease remains largely unknown. We conducted a genome-wide analysis to identify differentially methylated genes in vulnerable and non-vulnerable atherosclerotic lesions to understand more about pathogenesis.

resultsWe compared genome-wide DNA methylation profiling between carotid artery plaques of patients with clinically symptomatic (recent stroke or transient ischemic attack) and asymptomatic disease (no recent stroke) using Infinium Methylation BeadChip arrays, which revealed 90,368 differentially methylated sites (FDR < 0.05, |delta beta|> 0.03) corresponding to 14,657 annotated genes. Among these genomic sites, 30% were located at the promoter regions and 14% in the CpG islands, according to genomic loci and genomic proximity to the CpG islands, respectively. Moreover, 67% displayed hypomethylation in symptomatic plaques, and the differentially hypomethylated genes were found to be involved in various aspects of inflammation. Subsequently, we focus on CpG islands and revealed 14,596 differentially methylated sites (|delta beta|> 0.1) located at the promoter regions of 7048 genes. Integrated analysis of methylation and gene expression profiles identified that 107 genes were hypomethylated in symptomatic plaques and showed elevated expression levels in both advanced plaques and ruptured plaques. The imprinted gene PLA2G7, which encodes lipoprotein-associated phospholipase A

conclusionExtensive DNA methylation modifications serve as a new and critical layer of biological regulation that contributes to atheroprogression and destabilization via inflammatory processes. Revelation of this hitherto unknown epigenetic regulatory mechanism could rejuvenate the prospects of Lp-PLA

Indexed as

Epigenesis, Genetic1-Alkyl-2-acetylglycerophosphocholine EsteraseAgedDNA MethylationGene Expression RegulationGenetic VariationGenome-Wide Association StudyHealthy VolunteersHumansMaleMiddle AgedPlaque, AtheroscleroticStroke1-Alkyl-2-acetylglycerophosphocholine EsteraseAtherosclerosisDNA methylationInflammationLipoprotein-associated phospholipase A2PLA2G7Plaque vulnerability

Identifiers

PMID34419168
PMCPMC8379831
OpenAlexW3194970856

What OpenQuestion holds

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LicenceCC BY
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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.