ArticleAtherosclerosis2019
Atherosclerosis-associated differentially methylated regions can reflect the disease phenotype and are often at enhancers.
Article in Atherosclerosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Multimodal landscape of atherosclerotic plaques: A spatial omics approach with mass spectrometry imaging.Analytica chimica acta · 2025Review
- Unveiling the Relation between Cellular Aging, Epigenetics and Cancer.Aging and disease · 2025Article
- Spatial multiomics atlas reveals smooth muscle phenotypic transformation and metabolic reprogramming in diabetic macroangiopathy.Cardiovascular diabetology · 2024Article
- Exploring regulatory mechanisms on miRNAs and their implications in inflammation-related diseases.Clinical and experimental medicine · 2024Review
- Long Non-coding RNA DNM3OS: Pathogenic Roles and Molecular Mechanisms in Pathophysiological Processes.Current medicinal chemistry · 2024Review
- DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy.Cell communication and signaling : CCS · 2023Review
- Review
- Article
- Making sense of the ageing methylome.Nature reviews. Genetics · 2022Review
- Emerging mechanisms of elastin transcriptional regulation.American journal of physiology. Cell physiology · 2022Review
- Differences in the expression of DNA methyltransferases and demethylases in leukocytes and the severity of pulmonary arterial hypertension between ethnic groups.Physiological reports · 2022Article
- Mammalian peroxidasin (PXDN): From physiology to pathology.Free radical biology & medicine · 2022Review
- Sustained Downregulation of Vascular Smooth Muscle Acta2 After Transient Angiotensin II Infusion: A New Model of "Vascular Memory".Frontiers in cardiovascular medicine · 2022Article
- DNA Methylation Aberrant in Atherosclerosis.Frontiers in pharmacology · 2022Review
- Lipid Phenotypes and DNA Methylation: a Review of the Literature.Current atherosclerosis reports · 2021Review
- Pathophysiology of Atherosclerotic Plaque Development-Contemporary Experience and New Directions in Research.International journal of molecular sciences · 2021Review
- Article
- Hypomethylation of Rnase6 Promoter Enhances Proliferation and Migration of Murine Aortic Vascular Smooth Muscle Cells and Aggravates Atherosclerosis in Mice.Frontiers in bioengineering and biotechnology · 2021Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsAtherosclerosis is a widespread and complicated disease involving phenotypic modulation and transdifferentiation of vascular smooth muscle cells (SMCs), the predominant cells in aorta, as well as changes in endothelial cells and infiltrating monocytes. Alterations in DNA methylation are likely to play central roles in these phenotypic changes, just as they do in normal differentiation and cancer.
methodsWe examined genome-wide DNA methylation changes in atherosclerotic aorta using more stringent criteria for differentially methylated regions (DMRs) than in previous studies and compared these DMRs to tissue-specific epigenetic features.
resultsWe found that disease-linked hypermethylated DMRs account for 85% of the total atherosclerosis-associated DMRs and often overlap aorta-associated enhancer chromatin. These hypermethylated DMRs were associated with functionally different sets of genes compared to atherosclerosis-linked hypomethylated DMRs. The extent and nature of the DMRs could not be explained as direct effects of monocyte/macrophage infiltration. Among the known atherosclerosis- and contractile SMC-related genes that exhibited hypermethylated DMRs at aorta enhancer chromatin were ACTA2 (aorta α2 smooth muscle actin), ELN (elastin), MYOCD (myocardin), C9orf3 (miR-23b and miR-27b host gene), and MYH11 (smooth muscle myosin). Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.
conclusionsWe provide evidence for atherosclerosis-linked DNA methylation changes in aorta SMCs that might help minimize or reverse the standard contractile character of many of these cells by down-modulating aorta SMC-related enhancers, thereby facilitating pro-atherosclerotic phenotypic changes in many SMCs.
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