Dataset Information

Vascular Cast to Program Antistenotic Hemodynamics and Remodeling of Vein Graft.

ABSTRACT: The structural stability of medical devices is established by managing stress distribution in response to organ movement. Veins abruptly dilate upon arterial grafting due to the mismatched tissue property, resulting in flow disturbances and consequently stenosis. Vascular cast is designed to wrap the vein-artery grafts, thereby adjusting the diameter and property mismatches by relying on the elastic fixity. Here, a small bridge connection in the cast structure serves as an essential element to prevent stress concentrations due to the improved elastic fixity. Consequently, the vein dilation is efficiently suppressed, healthy (laminar and helical) flow is induced effectively, and the heathy functions of vein grafting are promoted, as indicated by the flow directional alignment of endothelial cells with arterialization, muscle expansion, and improved contractility. Finally, collaborative effects of the bridge drastically suppress stenosis with patency improvement. As a key technical point, the advantages of the bridge addition are validated via the computational modeling of fluid-structure interaction, followed by a customized ex vivo set-up and analyses. The calculated effects are verified using a series of cell, rat, and canine models towards translation. The bridge acted like "Little Dutch boy" who saved the big mass using one finger by supporting the cast function.

SUBMITTER: Ha H

PROVIDER: S-EPMC10074125 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature

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Publications

Vascular Cast to Program Antistenotic Hemodynamics and Remodeling of Vein Graft.

Ha Hyunsu H Park Ju Young JY Lee Chan Hee CH Son Deok-Hyeon DH Chung Soon Won SW Baek Sewoom S Lee Kyubae K Lee Kang Suk KS Yi Se Won SW Kang Mi-Lan ML Kim Dae-Hyun DH Sung Hak-Joon HJ

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20230202 10

The structural stability of medical devices is established by managing stress distribution in response to organ movement. Veins abruptly dilate upon arterial grafting due to the mismatched tissue property, resulting in flow disturbances and consequently stenosis. Vascular cast is designed to wrap the vein-artery grafts, thereby adjusting the diameter and property mismatches by relying on the elastic fixity. Here, a small bridge connection in the cast structure serves as an essential element to p ...[more]

PMID: 36727829

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Project description:Vein graft (VG) failure (VGF) is associated with VG intimal hyperplasia, which is characterized by abnormal accumulation of vascular smooth muscle cells (VSMCs). Most neointimal VSMCs are derived from pre-existing VSMCs via a process of VSMC phenotypic transition, also known as dedifferentiation. There is increasing evidence to suggest that ginger or its bioactive ingredients may block VSMC dedifferentiation, exerting vasoprotective functions; however, the precise mechanisms have not been fully characterized. Therefore, we investigated the effect of ginger on VSMC phenotypic transition in VG remodeling after transplantation. Ginger significantly inhibited neointimal hyperplasia and promoted lumen (L) opening in a 3-month VG, which was primarily achieved by reducing ferroptotic stress. Ferroptotic stress is a pro-ferroptotic state. Contractile VSMCs did not die but instead gained a proliferative capacity and switched to the secretory type, forming neointima (NI) after vein transplantation. Ginger and its two main vasoprotective ingredients (6-gingerol and 6-shogaol) inhibit VSMC dedifferentiation by reducing ferroptotic stress. Network pharmacology analysis revealed that 6-gingerol inhibits ferroptotic stress by targeting P53, while 6-shogaol inhibits ferroptotic stress by targeting 5-lipoxygenase (Alox5), both promoting ferroptosis. Furthermore, both ingredients co-target peroxisome proliferator-activated receptor gamma (PPARγ), decreasing PPARγ-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (Nox1) expression. Nox1 promotes intracellular reactive oxygen species (ROS) production and directly induces VSMC dedifferentiation. In addition, Nox1 is a ferroptosis-promoting gene that encourages ferroptotic stress production, indirectly leading to VSMC dedifferentiation. Ginger, a natural multi-targeted ferroptotic stress inhibitor, finely and effectively prevents VSMC phenotypic transition and protects against venous injury remodeling.

Dataset Information

Vascular Cast to Program Antistenotic Hemodynamics and Remodeling of Vein Graft.

Publications

Vascular Cast to Program Antistenotic Hemodynamics and Remodeling of Vein Graft.

Similar Datasets

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