ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Established neointimal hyperplasia in vein grafts expands via TGF-beta-mediated progressive fibrosis.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 55 citations in OpenAlex.
- Molecular Mechanisms of Intimal Hyperplasia in Saphenous Vein Grafts After Coronary Artery Bypass Grafting.Cells · 2026Review
- Blockade of YAP Mechanoactivation Prevents Neointima Formation and Adverse Remodeling in Arterialized Vein Grafts.Journal of the American Heart Association · 2025Article
- Nano-based perivascular intervention sustains a nine-month long-term suppression of intimal hyperplasia in vein grafts.Bioactive materials · 2025Article
- Markers of Restenosis after Percutaneous Transluminal Balloon Angioplasty in Patients with Critical Limb Ischemia.International journal of molecular sciences · 2023Review
- Sirolimus-Embedded Silk Microneedle Wrap to Prevent Neointimal Hyperplasia in Vein Graft Model.International journal of molecular sciences · 2023Article
- Translational model of vein graft failure following coronary artery bypass graft in atherosclerotic microswine.General thoracic and cardiovascular surgery · 2022Article
- Challenges and strategies forBioactive materials · 2021Review
- Treg cells in atherosclerosis.Molecular biology reports · 2021Review
- Interfering in the ALK1 Pathway Results in Macrophage-Driven Outward Remodeling of Murine Vein Grafts.Frontiers in cardiovascular medicine · 2021Article
- A validated mouse model capable of recapitulating the protective effects of female sex hormones on ascending aortic aneurysms and dissections (AADs).Physiological reports · 2020Article
- Cyclophilin A contributes to aortopathy induced by postnatal loss of smooth muscle TGFBR1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The BD2 domain of BRD4 is a determinant in EndoMT and vein graft neointima formation.Cellular signalling · 2019Article
- TGFβ, smooth muscle cells and coronary artery disease: a review.Cellular signalling · 2019Review
- A biodegradable synthetic graft for small arteries matches the performance of autologous vein in rat carotid arteries.Biomaterials · 2018Article
- Differential gene expression patterns in vein regions susceptible versus resistant to neointimal hyperplasia.Physiological genomics · 2018Article
- Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018Review
- Versican is differentially regulated in the adventitial and medial layers of human vein grafts.PloS one · 2018Article
- TGF-β1 in Vascular Wall Pathology: Unraveling Chronic Venous Insufficiency Pathophysiology.International journal of molecular sciences · 2017Review
- The effects of indoxyl sulfate-induced endothelial microparticles on neointimal hyperplasia formation in anAnnals of surgical treatment and research · 2017Article
- Smooth muscle cell-specific Tgfbr1 deficiency attenuates neointimal hyperplasia but promotes an undesired vascular phenotype for injured arteries.Physiological reports · 2016Article
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6 authors at 3 institutions in 1 country.
Funding
Abstract
In weeks to months following implantation, neointimal hyperplasia (NIH) in vein grafts (VGs) transitions from a cellularized to a decellularized phenotype. The inhibition of early cellular proliferation failed to improve long-term VG patency. We have previously demonstrated that transforming growth factor-beta(1) (TGF-beta(1))/connective tissue growth factor (CTGF) pathways mediate a conversion of fibroblasts to myofibroblasts in the early VG (<2 wk). We hypothesize that these similar pathways drive fibrosis observed in the late VG lesion. Within rabbit VGs, real-time RT-PCR, Western blot analysis, ELISA, and immunohistochemistry were used to examine TGF-beta/CTGF pathways in late (1-6 mo) NIH. All VGs exhibited a steady NIH growth (P = 0.006) with significant reduction in cellularity (P = 0.01) over time. Substantial TGF-beta profibrotic activities, as evidenced by enhanced TGF-beta(1) activation, TGF-beta receptor types I (activin receptor-like kinase 5)-to-II receptor ratio, SMAD2/3 phosphorylation, and CTGF production, persisted throughout the observation period. An increased matrix synthesis was accompanied by a temporal reduction of matrix metalloproteinase-2 (P = 0.001) and -9 (P < 0.001) activity. VG NIH is characterized by a conversion from a proproliferative to a profibrotic morphology. An enhanced signaling via TGF-beta/CTGF coupled with reduced matrix metalloproteinase activities promotes progressive fibrotic NIH expansion. The modulation of late TGF-beta/CTGF signaling may offer a novel therapeutic strategy to improve the long-term VG durability.
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