ArticleInternational journal of molecular sciences2023
Ant-Neointimal Formation Effects of SLC6A6 in Preventing Vascular Smooth Muscle Cell Proliferation and Migration via Wnt/β-Catenin Signaling.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- E2F5 Accelerates Vascular Smooth Muscle Cells Phenotype Switching in Diabetic Atherosclerosis through Activating Wnt/β-Catenin Pathway.Diabetes & metabolism journal · 2026Article
- DKK1/SMDT1 participate in Ang II-induced mitochondrial injury of human smooth muscle cells in an abdominal aortic aneurysm cell model.Experimental and therapeutic medicine · 2026Article
- Comprehensive Analysis of Bulk RNA-seq, Machine Learning, Mendelian Randomization, and Single-Cell Sequencing Unravels SLC22A3 as a Solute Carrier Superfamily-Associated Biomarker in Atherosclerosis.Journal of cardiovascular translational research · 2026Article
- Analysis of Transcriptome and Differentially Expressed Genes in Chicken Primordial Germ Cells.Animals : an open access journal from MDPI · 2026Article
- Prediction of cell states and key transcription factors of the human cornea through integrated single-cell omics analyses.PNAS nexus · 2025Article
- Hypotaurine Reduces Glucose-Mediated Vascular Calcification.Acta physiologica (Oxford, England) · 2025Article
- Taurine Alleviates Pancreatic β-Cell Senescence by Inhibition of p53 Pathway.Journal of diabetes · 2025Article
- Multimodal analysis of TAAD pathogenesis: SHAP-enhanced interpretable models and single-cell sequencing analysis reveal immune microenvironment alterations.Frontiers in immunology · 2025Article
- Identification of key genes associated with atrial fibrillation and hypoxia using WGCNA and machine learning technology.Frontiers in cardiovascular medicine · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of vascular remolding, such as atherosclerosis and restenosis. Solute carrier family 6 member 6 (SLC6A6) is a transmembrane transporter that maintains a variety of physiological functions and is highly expressed in VSMCs. However, its role on VSMCs during neointimal formation remains unknown. In this study, mRNA and protein levels of SLC6A6 were examined using models of VSMC phenotype switching in vivo and in vitro and human artery samples with or without atherosclerosis. SLC6A6 gain- and loss-of-function approaches were performed by adenovirus infection or small interfering RNA (siRNA) transfection, respectively. Reactive oxygen species (ROS), proliferation, migration, and phenotype-related proteins of VSMCs were measured. Vascular stenosis rate and related genes were assessed in a rat vascular balloon injury model overexpressing SLC6A6. SLC6A6 was downregulated in dedifferentiated VSMCs, atherosclerotic vascular tissues, and injured vascular tissues. SLC6A6 suppressed VSMC proliferation and migration, while increasing contractile VSMC proteins. Mechanistically, SLC6A6 overexpression reduced ROS production and inhibited the Wnt/β-catenin pathway. Furthermore, SLC6A6 overexpression suppressed neointimal formation in vivo. Collectively, overexpression of SLC6A6 suppresses neointimal formation by inhibiting VSMC proliferation and migration via Wnt/β-catenin signaling and maintaining the VSMC contractile phenotype.
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