ArticleArteriosclerosis, thrombosis, and vascular biology2025
Suv39h1 Regulates Phenotypic Modulation of Smooth Muscle Cells and Contributes to Vascular Injury by Repressing HIC1 Transcription.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- tRNA-derived small RNAs in vascular smooth muscle cell phenotypic switching and vascular remodelling.Molecular biology reports · 2026Review
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Glymphatic system impairment in neurological disorders: potential mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- The Complex Role of Methylation in Regulating Vascular Smooth Muscle Cell Phenotypic States in Vascular Remodeling and Atherosclerosis.Biomolecules · 2026Review
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Dynamic Balance of Histone H3 Methylation: Regulatory Mechanisms and Therapeutic Prospects in RA Immune Dysregulation and Bone Metabolism Imbalance.Journal of immunology research · 2026Review
- Role of histone post-translational modifications in atherosclerosis and the therapeutic potential of targeting epigenetic modifiers.Frontiers in cell and developmental biology · 2025Review
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8 authors.
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Abstract
backgroundVascular smooth muscle cells (VSMCs), in response to a myriad of injurious stimuli, switch from a contractile state to a proliferative/migratory state in a process known as phenotypic modulation. Phenotypic modulation of VSMCs contributes to neointima formation and underscores a host of vascular pathologies, including atherosclerosis. In the present study, we investigated the involvement of Suv39h1 (suppressor of variegation 3-9 homolog 1), a lysine methyltransferase, in this process.
methods
resultsSuv39h1 upregulation was observed in animal and cell models of phenotypic modulation. Consistently, Suv39h1 silencing restored expression of contractile genes and attenuated proliferation/migration in VSMCs exposed to PDGF (platelet-derived growth factor)-BB. Importantly, Suv39h1 deletion significantly ameliorated neointima formation in mice in both the carotid artery injury model and the femoral artery injury model. Importantly, a small-molecule Suv39h1 inhibitor F5446 suppressed phenotypic modulation in vitro and mitigated vascular injury in mice. RNA sequencing identified HIC1 (hypermethylated in cancer 1) as a novel target for Suv39h1. HIC1 expression was repressed by Suv39h1 during VSMC phenotypic modulation, whereas HIC1 overexpression antagonized neointima formation in mice. Integrated transcriptomic analysis indicated that HIC1 might regulate VSMC phenotypic modulation by activating Jag1 (Jagged 1) transcription.
conclusionsOur data suggest that Suv39h1 is a novel regulator of vascular injury and can be targeted for intervention of restenosis.
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