Evidence map›Paper›PMID 40606664›Full record

ArticleFrontiers in genetics2025

Epigenetic mechanisms linking atherosclerosis to ischemic stroke: insights from DNA methylation and transcriptome integration.

Binrong Ding, Yiqun Wang, Junfeng Li, Xuewei Zhang, Zhengqing Wan, Hao Wang

Abstract read
In one paragraph

Article in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Binrong DingPeople's Hospital of Ningxiang City, Hunan University of Chinese Medicine, Changsha, China.
Yiqun WangDepartment of Geriatrics, The Third Xiangya Hospital of Central South University, Changsha, China.
Junfeng LiPeople's Hospital of Ningxiang City, Hunan University of Chinese Medicine, Changsha, China.
Xuewei ZhangHealth Management Center, Xiangya Hospital, Central South University, Changsha, China.
Zhengqing WanDepartment of Medical Genetics, NHC Key Laboratory of Birth Defect for Research and Prevention, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, China.
Hao WangPeople's Hospital of Ningxiang City, Hunan University of Chinese Medicine, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Ischemic stroke (IS) is a major cause of mortality and disability, with atherosclerosis (AS) as a primary risk factor. DNA methylation plays a critical role in AS development, but its regulatory mechanisms remain unclear. This study aims to investigate the epigenetic regulatory mechanisms linking AS and IS by integrating DNA methylation and transcriptome data from public databases. Methods: This study integrated DNA methylation (GSE46394) and transcriptome data (GSE111782 and GSE162955) from public databases to investigate the molecular mechanisms linking AS and IS. Differentially methylated CpG positions (DMPs) and differentially expressed genes (DEGs) were identified (p < 0.05). Subsequent gene annotation and enrichment analyses were performed to uncover potential molecular mechanisms underlying the relationship between AS and IS. Results: A total of 5,396 consistent DMPs were identified in aortic and carotid atherosclerotic lesions, with enriched pathways such as MAPK signaling and Hippo signaling. Transcriptome analysis revealed 1,147 DEGs in AS plaques and 1,321 DEGs in IS brain tissues, enriched in pathways including neuroactive ligand-receptor interactions, calcium signaling, and vascular smooth muscle contraction. Overlapping analyses identified shared processes like actin filament polymerization, cell migration, and MAPK cascade regulation, as well as pathways such as adrenergic signaling, and apelin signaling. Conclusion: This study highlights the pivotal role of epigenetic regulation in AS and IS, uncovering key pathways and molecular processes involved in their progression. Future studies should validate these findings in larger cohorts and integrate multi-omics approaches for a comprehensive understanding.

Indexed as

atherosclerosisDNA methylationepigenetic regulationintegrated bioinformatics approachesischemic stroketranscriptomics

Identifiers

PMID40606664
PMCPMC12213582

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