ArticleArteriosclerosis, thrombosis, and vascular biology2020
Mature Vascular Smooth Muscle Cells, but Not Endothelial Cells, Serve as the Major Cellular Source of Intimal Hyperplasia in Vein Grafts.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Long-term remodeling of compliance matched tissue engineered vascular grafts is sex specific.Acta biomaterialia · 2026Article
- A Comprehensive Review of Epigenetic Regulation of Vascular Smooth Muscle Cells During Development and Disease.Biomolecules · 2026Review
- Bioinformatics and systems biology to identify underlying common pathogenesis of diabetic kidney disease and stenosis of arteriovenous fistula.BMC nephrology · 2025Article
- Vascular Smooth Muscle Cell Migration and P70S6K: Key Players in Intimal Hyperplasia Development.Journal of the American Heart Association · 2025Article
- Nanomedicine-based strategies for the treatment of vein graft disease.Nature reviews. Cardiology · 2025Review
- Ginger protects against vein graft remodeling by precisely modulating ferroptotic stress in vascular smooth muscle cell dedifferentiation.Journal of pharmaceutical analysis · 2025Article
- HnRNPA1 Prevents Endothelial-to-mesenchymal Transition-induced VSMC Activation and Neointimal Hyperplasia in Vein Grafts.Journal of cardiovascular translational research · 2024Article
- Targeted NADJournal of controlled release : official journal of the Controlled Release Society · 2024Article
- Fhl1, a new spatially specific protein, regulates vein graft neointimal hyperplasia.Clinical and translational medicine · 2024Article
- A bypass flow model to study endothelial cell mechanotransduction across diverse flow environments.Materials today. Bio · 2024Article
- Early Injury Landscape in Vein Harvest by Single-Cell and Spatial Transcriptomics.Circulation research · 2024Article
- Integrated single-nuclei and spatial transcriptomic analysis reveals propagation of early acute vein harvest and distension injury signaling pathways following arterial implantation.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic strategies based on non-ionizing radiation to prevent venous neointimal hyperplasia: the relevance for stenosed arteriovenous fistula, and the role of vascular compliance.Frontiers in cardiovascular medicine · 2024Review
- Neointima abating and endothelium preserving - An adventitia-localized nanoformulation to inhibit the epigenetic writer DOT1L.Biomaterials · 2023Article
- miR579-3p is an inhibitory modulator of neointimal hyperplasia and transcription factors c-MYB and KLF4.Cell death discovery · 2023Article
- Multilineage commitment of Sca-1Theranostics · 2023Article
- Nrf2-Mediated Dichotomy in the Vascular System: Mechanistic and Therapeutic Perspective.Cells · 2022Review
- IMP3 promotes re-endothelialization after arterial injury via increasing stability of VEGF mRNAhv.Journal of cellular and molecular medicine · 2022Article
- Article
- Fate and State of Vascular Smooth Muscle Cells in Atherosclerosis.Circulation · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveNeointima formation is a primary cause of intermediate to late vein graft (VG) failure. However, the precise source of neointima cells in VGs remains unclear. Approach and Results: Herein we clarify the relative contributions of mature vascular smooth muscle cells (SMCs) and endothelial cells (ECs) to neointima formation in a mouse model of VG remodeling via the genetic-inducible fate mapping approaches. Regardless of the magnitude of neointima formation, the recipient arterial and the donor venous SMCs contributed ≈55% of the neointima cells at the anastomotic regions, whereas only donor venous SMCs donated ≈68% of the neointima cells at the middle bodies. A small portion of the SMC-derived cells became non-SMC cells, most likely vascular stem cells, and constituted 2% to 11% of the cells in each major layer of VGs. In addition, the recipient arterial ECs were the major cellular source of re-endothelialization but did not contribute to neointima formation. The donor venous ECs donated ≈17% neointima cells in the VGs with mild neointima formation and conditional media from ECs after endothelial-to-mesenchymal transition suppressed vascular SMC dedifferentiation.
conclusionsThe recipient arterial and donor venous mature SMCs dominate but contribute distinctly to intimal hyperplasia at the anastomosis and the middle body regions of VGs. The recipient arterial ECs are the major cellular source of re-endothelialization but do not donate neointima formation in VGs. Only the donor venous ECs undergo endothelial-to-mesenchymal transition. Endothelial-to-mesenchymal transition is marginal for generating neointima cells but is likely required for controlling the quality of VG remodeling.
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