Evidence map›Paper›PMID 35227297›Full record

ArticleClinical epigenetics2022

Atheroprotective mechanism by which folic acid regulates monocyte subsets and function through DNA methylation.

Yang Xiang, Bin Liang, Xiaokang Zhang, Xueping Qiu, Qianyun Deng, Li Yu, Hong Yu, Zhibing Lu, Fang Zheng

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  16. Biofilm · 2023
    Article
  17. Article
  18. The role of monocytes in thrombotic diseases: a review.Frontiers in cardiovascular medicine · 2023
    Review
  19. Review
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

9 authors at 2 institutions in 1 country.

Yang Xiang *Center for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Bin Liang *Center for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Xiaokang Zhang *Center for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Xueping QiuCenter for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Qianyun DengLaboratory Medicine, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Li YuCenter for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Hong YuHubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan University School of Basic Medical Sciences, Wuhan, 430071, Hubei, China.
Zhibing LuInstitute of Myocardial Injury and Repair, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China.
Fang ZhengCenter for Gene Diagnosis, and Department of Clinical Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. zhengfang@whu.edu.cn.ORCID 0000-0002-2024-2424
Wuhan University · CNGuangdong Academy of Medical Sciences · CN

Funding

National Natural Science Foundation of China 81871722National Natural Science Foundation of China 82002235National Natural Science Foundation of China 82072373
6 · The paper itself

Abstract

backgroundRecent studies have suggested that folic acid can restore abnormal DNA methylation and monocyte subset shifts caused by hyperhomocysteinemia (HHcy) and hyperlipidemia (HL). However, the exact mechanism of action is still not fully understood. In this study, we further investigated the reversal effect and underlying mechanism of folic acid on the shift in monocyte subsets induced by aberrant lipids and Hcy metabolism via DNA methylation in vitro and in vivo.

resultsOur results showed that intermediate monocytes were significantly increased but had the lowest global 5-methylcytosine (5-mC) levels in coronary artery disease (CAD) patients, which might lead to a decrease in the global 5-mC levels of peripheral blood leukocytes (PBLs). We also discovered that ARID5B might mediate the increased proportion of intermediate monocytes, as this factor was related to the proportion of monocyte subsets and the expression of CCR2. The expression of ARID5B was inversely associated with the hypermethylated cg25953130 CpG site, which was induced by HL and HHcy. ARID5B could also regulate monocyte CCR2, MCP-1, and TNF-α expression, adhesion and migration, macrophage polarization, and monocyte/macrophage apoptosis, which might explain the regulatory effect of ARID5B on monocyte subset shifting. Folic acid reversed HL- and HHcy-mediated aberrant global and cg25953130 DNA methylation, reduced the proportion of intermediate monocytes, and inhibited the formation of atherosclerotic plaques.

conclusionFolic acid plays a protective role against atherosclerosis through the regulation of DNA methylation, ARID5B expression, and monocyte subsets.

Indexed as

AtherosclerosisPlaque, AtheroscleroticDNA MethylationFolic AcidHumansMonocytesFolic AcidARID5BCoronary artery diseaseDNA methylationFolic acidMonocyte subsets

Identifiers

PMID35227297
PMCPMC8887029
OpenAlexW4214542378

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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.