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Cardiovascular & Hematological Disorders-Drug Targets

Editor-in-Chief

ISSN (Print): 1871-529X
ISSN (Online): 2212-4063

Pathogenesis of Neointima Formation Following Vascular Injury

Author(s): Ali Pourdjabbar, Benjamin Hibbert, Trevor Simard and Xiaoli Ma

Volume 11, Issue 1, 2011

Page: [30 - 39] Pages: 10

DOI: 10.2174/187152911795945169

Price: $65

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


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