ArticleJournal of advanced research2026
Cytoskeletal-related genes function as checkpoints for the maintenance of VSMC contractile phenotype and prevent pathological remodeling in arterial diseases.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- tRNA-derived small RNAs in vascular smooth muscle cell phenotypic switching and vascular remodelling.Molecular biology reports · 2026Review
- Vascular Smooth Muscle Cell Plasticity in Atherosclerosis: Mechanisms, Recent Advances, and Therapeutic Implications.Reviews in cardiovascular medicine · 2026Review
- Re-analysis of single-cell transcriptomics reveals a critical role of TNS1 gene in driving contractile VSMC transdifferentiation into macrophage-like SMC and atherosclerotic plaque instability.Clinical and translational medicine · 2026Article
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionArterial pathological remodeling, central to arterial diseases including atherosclerosis and aortic aneurysms, is characterized by vascular smooth muscle cell (VSMC) phenotypic switching with concomitant loss of contractile markers. Uncovering the molecular changes initiating phenotypic transition may advance the understanding of vascular pathogenesis and provide new therapeutic strategies.
objectivesTo construct a cross-species integrative model of VSMC transition in arterial diseases including atherosclerosis and aortic aneurysm, identify key genes regulating phenotypic switching in the trajectory from contractile to other phenotypes, and further validate their function in arterial remodeling models.
methodsPublic single-cell RNA-seq datasets were analyzed to map VSMC transcriptional dynamics and identify regulated gene expression patterns during transition. The changes were further checked using experimental animal aneurysm samples and PDGF-BB treated VSMCs. Functional validation included in vitro siRNA-mediated knockdown using primary VSMCs and in vivo gene-manipulated (AAv-shRNA/Adv-overexpression) wire-injury models.
resultsDysregulation of cytoskeletal-related genes (Fblim1, Tns1, and Synpo2) may cause disarrangement of actin cytoskeleton, and were identified as checkpoint process before VSMCs transition initiation. Knockdown of target genes suppressed contractile markers, enhanced proliferation, migration, and disrupted cytoskeleton architecture in VSMCs. In animal models, gene down-regulation exacerbated pathological remodeling while over-expression partially reverted these effects.
conclusionThe findings highlight the critical role of cytoskeleton-related genes in arterial diseases that function as a critical checkpoint in preventing VSMC pathological phenotypic switching.
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