Atlas drug-eluting coronary stents inhibits neointimal hyperplasia in sheep modeling

Dinc, Rasit; Yerebakan, Halit

doi:10.1101/2023.04.19.537461

Cited by 1 publication

(2 citation statements)

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“…The formation of neointimal proliferation leading to in-stent restenosis (ISR) is a result of the response to injuries occurring after endovascular intervention. Although there is ISR due to neointimal proliferation after BA, this mechanism occurs more exaggeratedly in stent cases [ 6 8 9 ]. Drug-eluting stents (DES) have further reduced the rate of restenosis to < 10%, especially with the introduction of the second generation, a biodegradable and biocompatible polymer that provides controlled drug release, and a drug-coated balloon [ 10 11 ].…”

Section: Introductionmentioning

confidence: 99%

“…Drug-eluting stents (DES) have further reduced the rate of restenosis to < 10%, especially with the introduction of the second generation, a biodegradable and biocompatible polymer that provides controlled drug release, and a drug-coated balloon [ 10 11 ]. Although early elastic recoil and vascular remodeling were prevented to some extent by the stents, restenosis associated with neointimal hyperplasia could not be completely prevented in the long term [ 9 ]. The underlying mechanisms may induce factors associated with functional impairment of PAD, and a better understanding of these pathways may help guide new medical therapies for treatment [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

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A review of the current state in neointimal hyperplasia development following endovascular intervention and minor emphasis on new horizons in immunotherapy

Dinc

2023

Transl Clin Pharmacol

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Endovascular strategies play a vital role in the treatment of peripheral arterial disease (PAD). However, luminal loss or restenosis after endovascular intervention remains a significant challenge. The main underlying mechanisms are negative vascular remodeling and elastic recoil in balloon angioplasty. During stenting, the main reason for this complex is neointimal proliferation. Endothelial cell injury due to endovascular intervention initiates a series of molecular events, such as overexpression of growth factors, cytokine secretion, and adhesion molecules. These induce platelet activation and inflammatory processes, which trigger the proliferation and migration of vascular smooth muscle cells into the intima, resulting in neointimal hyperplasia. During this process, PAD progression is mainly caused by chronic inflammation, in which macrophages play a central role. Of the current strategies, drug release interventions aim to suppress restenosis using antiproliferative drugs, such as sirolimus and paclitaxel, during drug release. These drugs inhibit vascular reendothelialization and reduce late in-stent restenosis. For this reason, immunotherapy can be considered an important alternative. Interventions that polarize macrophages to the M2 subtype are particularly important, as they shape the immune response in an anti-inflammatory direction and contribute to tissue repair. However, there are several challenges to overcome, such as localizing antiproliferative or polarizing agents only to areas of vascular injury. This review discusses, based on the early study observations, immunotherapeutic approaches to prevent restenosis after endovascular intervention for the treatment of PAD.

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