Fracture of a popliteal nitinol stent and pseudoaneurysm: a case report and review of the literature

Reis, José Maciel Caldas dos; Kudo, Fabio A.; Bastos, Moisés do Carmo

doi:10.1093/jscr/rjz312

Cited by 4 publications

(1 citation statement)

References 10 publications

(17 reference statements)

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“…Due to the mechanical nature of the leg, stents can become cracked, promote artery kinking, and result in pseudoaneurysms. [47][48][49] As such, a systemically deliverable drug that can block SMC restenosis following percutaneous transluminal angioplasty could prove significantly beneficial to patients.…”

Section: Discussionmentioning

confidence: 99%

FAK Activation Promotes SMC Dedifferentiation via Increased DNA Methylation in Contractile Genes

Jeong

Murphy

Kim

et al. 2021

Circulation Research

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Rationale: Vascular smooth muscle cells (SMCs) exhibit remarkable plasticity and can undergo dedifferentiation upon pathological stimuli associated with disease and interventions. Objective: Although epigenetic changes are critical in SMC phenotype switching, a fundamental regulator that governs the epigenetic machineries regulating the fate of SMC phenotype has not been elucidated. Methods and Results: Using SMCs, mouse models, and human atherosclerosis specimens, we found that FAK (focal adhesion kinase) activation elicits SMC dedifferentiation by stabilizing DNMT3A (DNA methyltransferase 3A). FAK in SMCs is activated in the cytoplasm upon serum stimulation in vitro or vessel injury and active FAK prevents DNMT3A from nuclear FAK-mediated degradation. However, pharmacological or genetic FAK catalytic inhibition forced FAK nuclear localization, which reduced DNMT3A protein via enhanced ubiquitination and proteasomal degradation. Reduced DNMT3A protein led to DNA hypomethylation in contractile gene promoters, which increased SMC contractile protein expression. RNA-sequencing identified SMC contractile genes as a foremost upregulated group by FAK inhibition from injured femoral artery samples compared with vehicle group. DNMT3A knockdown in injured arteries reduced DNA methylation and enhanced contractile gene expression supports the notion that nuclear FAK-mediated DNMT3A degradation via E3 ligase TRAF6 (TNF [tumor necrosis factor] receptor-associated factor 6) drives differentiation of SMCs. Furthermore, we observed that SMCs of human atherosclerotic lesions exhibited decreased nuclear FAK, which was associated with increased DNMT3A levels and decreased contractile gene expression. Conclusions: This study reveals that nuclear FAK induced by FAK catalytic inhibition specifically suppresses DNMT3A expression in injured vessels resulting in maintaining SMC differentiation by promoting the contractile gene expression. Thus, FAK inhibitors may provide a new treatment option to block SMC phenotypic switching during vascular remodeling and atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

FAK Activation Promotes SMC Dedifferentiation via Increased DNA Methylation in Contractile Genes

Jeong

Murphy

Kim

et al. 2021

Circulation Research

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Effect of balloon pre-dilation on performance of self-expandable nitinol stent in femoropopliteal artery

Zhao

Silberschmidt

2022

Biomech Model Mechanobiol

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Balloon pre-dilation is usually performed before implantation of a nitinol stent in a femoropopliteal artery in a case of severe blockage or calcified plaque. However, its effect on performance of the nitinol stent in a diseased femoropopliteal artery has not been studied yet. This study compares the outcomes of stenting with pre-dilation and without it by modelling the entire processes of stent deployment. Fatigue deformation of the implanted stent is also modelled under diastolic–systolic blood pressure, repetitive bending, torsion, axial compression and their combination. Reduced level of stress in the stent occurs after stenting with pre-dilation, but causing the increased damage in the media layer, i.e. the middle layer of the arterial wall. Generally, pre-dilation increases the risk of nitinol stent’s fatigue failure. Additionally, the development of in-stent restenosis is predicted based on the stenting-induced tissue damage in the media layer, and no severe mechanical irritation is induced to the media layer by pre-dilation, stent deployment or fatigue loading.

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Femoropopliteal Pseudoaneurysms as a Complication of Self-Expanding Nitinol Stent Fracture: A Brief Report and Review

Aten,

Gerlt,

Rosol

et al. 2024

The American Journal of Cardiology

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Fracture of a popliteal nitinol stent and pseudoaneurysm: a case report and review of the literature

Cited by 4 publications

References 10 publications

FAK Activation Promotes SMC Dedifferentiation via Increased DNA Methylation in Contractile Genes

FAK Activation Promotes SMC Dedifferentiation via Increased DNA Methylation in Contractile Genes

Effect of balloon pre-dilation on performance of self-expandable nitinol stent in femoropopliteal artery

Femoropopliteal Pseudoaneurysms as a Complication of Self-Expanding Nitinol Stent Fracture: A Brief Report and Review

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