Abstract
Revascularization remains the cornerstone of managing obstructive coronary artery disease. Although percutaneous coronary interventions involving the insertion of metal scaffolds, known as stents, has emerged as the preferred method of restoring vessel patency, as many as 30% of patients will experience a gradual re-narrowing of the lumen caused by neointima (NI) formation, resulting in a condition known as in-stent restenosis (ISR). ISR represents a significant limitation to percutaneous revascularization – however, abrogating NI formation following stent implantation has been hampered by an incomplete understanding of the pathogenesis of in-stent lesions. While numerous mechanisms have been proposed to explain the pathogenesis of ISR, data from human and animal models have yielded conflicting results. Herein, we review key studies of NI development following vascular injury with a focus on the origin of cells participating in NI formation.
Keywords: In-stent restenosis, neointima, smooth muscle cell, endothelial cell, vascular progenitor cell, endothelial progenitor cell, drug-eluting stents, hyperplasia, contractile phenotype
Cardiovascular & Hematological Disorders-Drug Targets
Title: Pathogenesis of Neointima Formation Following Vascular Injury
Volume: 11 Issue: 1
Author(s): Ali Pourdjabbar, Benjamin Hibbert, Trevor Simard and Xiaoli Ma
Affiliation:
Keywords: In-stent restenosis, neointima, smooth muscle cell, endothelial cell, vascular progenitor cell, endothelial progenitor cell, drug-eluting stents, hyperplasia, contractile phenotype
Abstract: Revascularization remains the cornerstone of managing obstructive coronary artery disease. Although percutaneous coronary interventions involving the insertion of metal scaffolds, known as stents, has emerged as the preferred method of restoring vessel patency, as many as 30% of patients will experience a gradual re-narrowing of the lumen caused by neointima (NI) formation, resulting in a condition known as in-stent restenosis (ISR). ISR represents a significant limitation to percutaneous revascularization – however, abrogating NI formation following stent implantation has been hampered by an incomplete understanding of the pathogenesis of in-stent lesions. While numerous mechanisms have been proposed to explain the pathogenesis of ISR, data from human and animal models have yielded conflicting results. Herein, we review key studies of NI development following vascular injury with a focus on the origin of cells participating in NI formation.
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Cite this article as:
Pourdjabbar Ali, Hibbert Benjamin, Simard Trevor and Ma Xiaoli, Pathogenesis of Neointima Formation Following Vascular Injury, Cardiovascular & Hematological Disorders-Drug Targets 2011; 11 (1) . https://dx.doi.org/10.2174/187152911795945169
DOI https://dx.doi.org/10.2174/187152911795945169 |
Print ISSN 1871-529X |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-4063 |
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