ArticleThe Journal of clinical investigation2020
Smooth muscle cell-specific fibronectin-EDA mediates phenotypic switching and neointimal hyperplasia.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Splicing of fibronectin gene contribute to the aneurysmal dilatation of arteriovenous fistula.Renal failure · 2026Article
- Knockdown of DVL2 inhibits vascular smooth muscle cell proliferation and migration.Scientific reports · 2026Article
- Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling : EVs promote VSMC phenotypic switching.Cellular and molecular life sciences : CMLS · 2026Article
- FAK Differentially Mechanoregulates Cell Migration during Wound Closure.ACS biomaterials science & engineering · 2025Article
- NEXN regulates vascular smooth muscle cell phenotypic switching and neointimal hyperplasia.JCI insight · 2025Article
- Smooth Muscle Cell-Derived Fibronectin Promotes an Atheroprotective Smooth Muscle Cell Phenotype Associated With Altered NO-cGMP Signaling.Journal of the American Heart Association · 2025Article
- Deletion of smooth muscle ZFP36 promotes neointimal hyperplasia in mice.Acta pharmacologica Sinica · 2025Article
- FAK Differentially Mechanoregulates Cell Migration During Wound Closure.bioRxiv : the preprint server for biology · 2025Article
- Intravascular delivery of an MK2 inhibitory peptide to prevent restenosis after angioplasty.Biomaterials · 2025Article
- Exosomes in arteriovenous fistula stenosis.Frontiers in cell and developmental biology · 2025Review
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
- 3D confinement alters smooth muscle cell responses to chemical and mechanical cues.APL bioengineering · 2024Article
- Influence of DNA Methylation on Vascular Smooth Muscle Cell Phenotypic Switching.International journal of molecular sciences · 2024Review
- Fabrication of 3D Biomimetic Smooth Muscle Using Magnetic Induction and Bioprinting for Tissue Regeneration.Biomaterials research · 2024Article
- Smooth muscle cell phenotypic switching occurs independent of aortic dilation in bicuspid aortic valve-associated ascending aortas.PloS one · 2024Article
- Promotion of uterine reconstruction by a tissue-engineered uterus with biomimetic structure and extracellular matrix microenvironment.Science advances · 2023Article
- Neointima abating and endothelium preserving - An adventitia-localized nanoformulation to inhibit the epigenetic writer DOT1L.Biomaterials · 2023Article
- Sinus venosus adaptation models prolonged cardiovascular disease and reveals insights into evolutionary transitions of the vertebrate heart.Nature communications · 2023Article
- Extracellular Matrix Remodeling in Vascular Disease: Defining Its Regulators and Pathological Influence.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors.Journal of nanobiotechnology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Fibronectin-splice variant containing extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury. The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointimal hyperplasia remains unclear. Herein, using human coronary artery sections with a bare metal stent, we demonstrate the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas. In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperlipidemia by potentiating SMC proliferation and migration. No sex-based differences were observed. Mechanistic studies suggested that Fn-EDA mediates integrin- and TLR4-dependent proliferation and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively. Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with decreased Akt1/mTOR signaling. Targeting Fn-EDA in human aortic SMCs suppressed the synthetic phenotype and downregulated Akt1/mTOR signaling. These results reveal that SMC-derived Fn-EDA potentiates phenotypic switching in human and mouse aortic SMCs and neointimal hyperplasia in the mouse. We suggest that targeting Fn-EDA could be explored as a potential therapeutic strategy to reduce neointimal hyperplasia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.