ArticleArteriosclerosis, thrombosis, and vascular biology2019
Epigenetic Regulation of Vascular Smooth Muscle Cells by Histone H3 Lysine 9 Dimethylation Attenuates Target Gene-Induction by Inflammatory Signaling.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- The Complex Role of Methylation in Regulating Vascular Smooth Muscle Cell Phenotypic States in Vascular Remodeling and Atherosclerosis.Biomolecules · 2026Review
- N6-methyladenosine (m6A) post-transcriptional modification regulation of mRNA, an overlooked therapeutic opportunity to leverage mRNA processing in vascular smooth muscle cells.Vascular pharmacology · 2026Review
- EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G.Experimental & molecular medicine · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Epigenetic Regulation and Molecular Mechanisms in Cardiovascular Diseases: A Review of Recent Advances and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Matrix metalloproteinase-12 in arterial diseases: context-dependent mechanisms of vascular remodeling and therapeutic implications.Frontiers in cardiovascular medicine · 2026Review
- Vascular Smooth Muscle Cell Metabolic Disorders in the Occurrence and Development of Aortic Aneurysms and Dissections: Implications for Therapy.Biomedicines · 2025Review
- Endothelial cells retain inflammatory memory through chromatin remodeling in a two-hit model of infection-induced inflammation.American journal of physiology. Cell physiology · 2025Article
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
- Advances in brain remodeling, stem cell therapies, and translational barriers in stroke and brain aging.Biogerontology · 2025Review
- LncRNA PVT1 Facilitates Phenotypic Switching of Vascular Smooth Muscle Cells in Intracranial Aneurysms by Recruiting KDM1A to Reduce H3K9me2 Modification.The Kaohsiung journal of medical sciences · 2025Article
- Understanding residual risk of cardiovascular disease in people with HIV.Current opinion in HIV and AIDS · 2025Review
- SET7 lysine methyltransferase mediates the up-regulation of NADPH oxidase expression, oxidative stress, and NLRP3 inflammasome priming in atherosclerosis.Journal of translational medicine · 2025Article
- Enrichment of H3S28p and H3K9me2 Epigenetic Marks on Inflammatory-Associated Gene Promoters in Response to Severe Burn Injury.Life (Basel, Switzerland) · 2024Article
- Mechanism and application of feedback loops formed by mechanotransduction and histone modifications.Genes & diseases · 2024Review
- Nuclear Control of Vascular Smooth Muscle Cell Plasticity during Vascular Remodeling.The American journal of pathology · 2024Review
- Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- BACH1 deficiency prevents neointima formation and maintains the differentiated phenotype of vascular smooth muscle cells by regulating chromatin accessibility.Nucleic acids research · 2023Article
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15 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveVascular inflammation underlies cardiovascular disease. Vascular smooth muscle cells (VSMCs) upregulate selective genes, including MMPs (matrix metalloproteinases) and proinflammatory cytokines upon local inflammation, which directly contribute to vascular disease and adverse clinical outcome. Identification of factors controlling VSMC responses to inflammation is therefore of considerable therapeutic importance. Here, we determine the role of Histone H3 lysine 9 di-methylation (H3K9me2), a repressive epigenetic mark that is reduced in atherosclerotic lesions, in regulating the VSMC inflammatory response. Approach and Results: We used VSMC-lineage tracing to reveal reduced H3K9me2 levels in VSMCs of arteries after injury and in atherosclerotic lesions compared with control vessels. Intriguingly, chromatin immunoprecipitation showed H3K9me2 enrichment at a subset of inflammation-responsive gene promoters, including
conclusionsThis study implicates H3K9me2 in regulating the proinflammatory VSMC phenotype. Our findings suggest that reduced H3K9me2 in disease enhance binding of NFκB and AP-1 (activator protein-1) transcription factors at specific inflammation-responsive genes to augment proinflammatory stimuli in VSMC. Therefore, H3K9me2-regulation could be targeted clinically to limit expression of MMPs and IL6, which are induced in vascular disease.
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