Evidence map›Paper›PMID 39627020›Full record

ArticleEpigenetics2024

Homocysteine affects macrophage polarization by altering m6A methylation of scavenger receptors CD209 and CD163L1.

Yu Liang, Yongbo Wang, Jia Tan, Jingxuan Shu, Ya Xu, Mingyuan Wang, Shengjun Yang, Linna Ma

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Epigenetics, 2024. 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

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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. 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

8 authors.

Yu LiangDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Yongbo WangDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Jia TanDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Jingxuan ShuDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Ya XuDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Mingyuan WangDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Shengjun YangDepartment of Clinical Laboratory, The First People's Hospital of Yunnan Province, Kunming, Yunnan, P.R. China.
Linna MaDepartment of Medical Laboratory Technique, Kunming Medical University Haiyuan College, Kunming, Yunnan, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease characterized by fatty plaque deposits on artery walls. Elevated plasma homocysteine (Hcy) levels are an independent risk factor for atherosclerosis. Research on the mechanism by which Hcy promotes atherosclerosis has gradually turned to epigenetic inheritance, but the correlation between Hcy and m6A (N6-methyladenosine) modification has not been reported. In this study, MeRIP-seq was performed on macrophages and Hcy-treated macrophages. GO and KEGG analyses were used to perform functional analysis of differentially methylated genes. qRT-PCR and western blot were taken to determine the expression of CD209, CD163L1, proinflammatory, and anti-inflammatory factors. Flow cytometry was used to detect the proportion of M2 macrophages. The results showed that after Hcy treatment, the overall m6A methylation of macrophages was down-regulated, and 856 differential methylation peaks were annotated to 781 genes. These included CD209 and CD163L1, whose m6A methylation was inhibited after treatment with Hcy. In addition, mRNA and protein expressions of CD209 and CD163L1 were also inhibited after Hcy treatment. Overexpression of CD209 or CD163L1 prevents the Hcy-induced decrease in the proportion of M2 macrophages. This article identified changes in the modification level of m6A in macrophages by Hcy and revealed the possible mechanism by which Hcy induces macrophage polarization.

Indexed as

HomocysteineMacrophagesReceptors, Cell SurfaceAdenosineAnimalsCell Adhesion MoleculesDC-Specific ICAM-3 Grabbing NonintegrinEpigenesis, GeneticHumansLectins, C-TypeMethylationMiceAdenosineCell Adhesion MoleculesDC-Specific ICAM-3 Grabbing NonintegrinHomocysteineLectins, C-TypeN-methyladenosineReceptors, Cell SurfaceAtherosclerosisCD163L1CD209homocysteinem6A methylation

Identifiers

PMID39627020
PMCPMC11622620

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