ArticleJVS-vascular science2020
Transcriptomic profiling of experimental arterial injury reveals new mechanisms and temporal dynamics in vascular healing response.
Article in JVS-vascular science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- FOXC1 Controls Smooth Muscle Cell Differentiation and Plasticity in Vascular Disease.JACC. Basic to translational science · 2026Article
- Multi-omics data integration from patients with carotid stenosis illuminates key molecular signatures of atherosclerotic instability.Genome medicine · 2026Article
- Thrombospondin-4 regulates apoptosis of vascular smooth muscle cells after artery transplanted into vein.Scientific reports · 2025Article
- Atheroma transcriptomics identifies ARNTL as a smooth muscle cell regulator and with clinical and genetic data improves risk stratification.European heart journal · 2025Article
- Dysregulation of MMP2-dependent TGF-ß2 activation impairs fibrous cap formation in type 2 diabetes-associated atherosclerosis.Nature communications · 2024Article
- Transcriptomic and physiological analyses reveal temporal changes contributing to the delayed healing response to arterial injury in diabetic rats.JVS-vascular science · 2023Article
- Article
- Vascular smooth muscle cells in atherosclerosis: time for a re-assessment.Cardiovascular research · 2021Review
- Article
- Great start predicts bright future forJVS-vascular science · 2021Article
- AMPA-Type Glutamate Receptors Associated With Vascular Smooth Muscle Cell Subpopulations in Atherosclerosis and Vascular Injury.Frontiers in cardiovascular medicine · 2021Article
- Back to the future but better.JVS-vascular science · 2020Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEndovascular interventions cause arterial injury and induce a healing response to restore vessel wall homeostasis. Complications of defective or excessive healing are common and result in increased morbidity and repeated interventions. Experimental models of intimal hyperplasia are vital for understanding the vascular healing mechanisms and resolving the clinical problems of restenosis, vein graft stenosis, and dialysis access failure. Our aim was to systematically investigate the transcriptional, histologic, and systemic reaction to vascular injury during a prolonged time.
methodsBalloon injury of the left common carotid artery was performed in male rats. Animals (n = 69) were euthanized before or after injury, either directly or after 2 hours, 20 hours, 2 days, 5 days, 2 weeks, 6 weeks, and 12 weeks. Both injured and contralateral arteries were subjected to microarray profiling, followed by bioinformatic exploration, histologic characterization of the biopsy specimens, and plasma lipid analyses.
resultsImmune activation and coagulation were key mechanisms in the early response, followed by cytokine release, tissue remodeling, and smooth muscle cell modulation several days after injury, with reacquisition of contractile features in later phases. Novel pathways related to clonal expansion, inflammatory transformation, and chondro-osteogenic differentiation were identified and immunolocalized to neointimal smooth muscle cells. Analysis of uninjured arteries revealed a systemic component of the reaction after local injury, underlined by altered endothelial signaling, changes in overall tissue bioenergy metabolism, and plasma high-density lipoprotein levels.
conclusionsWe demonstrate that vascular injury induces dynamic transcriptional landscape and metabolic changes identifiable as early, intermediate, and late response phases, reaching homeostasis after several weeks. This study provides a temporal "roadmap" of vascular healing as a publicly available resource for the research community.
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