ArticleNucleic acids research2023
BACH1 deficiency prevents neointima formation and maintains the differentiated phenotype of vascular smooth muscle cells by regulating chromatin accessibility.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 33 citations in OpenAlex.
- Losartan Ameliorates Coronary Neointimal Thickening in a Mouse Model of Kawasaki Disease: A Pilot Study.Biomedicines · 2026Article
- PCSK5 promotes angiogenesis and cardiac repair after myocardial infarction.Nature communications · 2026Article
- Histone methyltransferase G9a drives vascular smooth muscle cell proliferation and intimal hyperplasia in mice.Acta pharmacologica Sinica · 2026Article
- EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G.Experimental & molecular medicine · 2026Article
- Targeting the Hippo pathway in pulmonary arterial hypertension: emerging pharmacological strategies.Journal of hypertension · 2026Review
- Article
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway.Frontiers in pharmacology · 2026Article
- Research progress on the molecular mechanisms of chlorogenic acid's pharmacological effects and its advanced drug delivery systems.Frontiers in pharmacology · 2026Review
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Article
- LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1.Journal of cellular and molecular medicine · 2025Article
- Coronary artery disease-associated variants regulate vascular smooth muscle cell gene expression.Nature cardiovascular research · 2025Article
- A BACH1 inhibitor ameliorates myocardial infarction and limb ischemia in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells.Stem cell research & therapy · 2025Article
- STAT3 Facilitates Super Enhancer Formation to Promote Fibroblast-To-Myofibroblast Differentiation by the Analysis of ATAC-Seq, RNA-Seq and ChIP-Seq.Journal of cellular and molecular medicine · 2025Review
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- O-GlcNAcylation-dependent liquid-liquid phase separation regulates the nuclear translocation of YAP to exacerbate vascular neointimal hyperplasia.Theranostics · 2025Article
- The interplay between hormonal vitamin D and lipopolysaccharide signaling on human neutrophil transcriptional responses.Frontiers in immunology · 2025Article
- MiR-196a-5p hinders vascular smooth muscle cell proliferation and vascular remodeling via repressing BACH1 expression.Scientific reports · 2024Article
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Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor BTB and CNC homology 1(BACH1) has been linked to coronary artery disease risk by human genome-wide association studies, but little is known about the role of BACH1 in vascular smooth muscle cell (VSMC) phenotype switching and neointima formation following vascular injury. Therefore, this study aims to explore the role of BACH1 in vascular remodeling and its underlying mechanisms. BACH1 was highly expressed in human atherosclerotic plaques and has high transcriptional factor activity in VSMCs of human atherosclerotic arteries. VSMC-specific loss of Bach1 in mice inhibited the transformation of VSMC from contractile to synthetic phenotype and VSMC proliferation and attenuated the neointimal hyperplasia induced by wire injury. Mechanistically, BACH1 suppressed chromatin accessibility at the promoters of VSMC marker genes via recruiting histone methyltransferase G9a and cofactor YAP and maintaining the H3K9me2 state, thereby repressing VSMC marker genes expression in human aortic smooth muscle cells (HASMCs). BACH1-induced repression of VSMC marker genes was abolished by the silencing of G9a or YAP. Thus, these findings demonstrate a crucial regulatory role of BACH1 in VSMC phenotypic transition and vascular homeostasis and shed light on potential future protective vascular disease intervention via manipulation of BACH1.
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