Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype

Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype

Summary: Even the most advanced drug-eluting stents evoke unresolved issues, including chronic inflammation, late thrombosis, and neoatherosclerosis. This highlights the need for novel strategies that improve stent biocompatibility. Our studies show that apolipoprotein A-I (apoA-I) reduces in-stent...

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Bibliographic Details
Main Authors: Laura Z. Vanags, PhD, Joanne T.M. Tan, PhD, Keyvan K. Galougahi, MD, PhD, Andreas Schaefer, MD, Steven G. Wise, PhD, Andrew Murphy, PhD, Ziad A. Ali, MD, PhD, Christina A. Bursill, PhD
Format: Article
Language:English
Published: Elsevier 2018-04-01
Series:JACC: Basic to Translational Science
Online Access:http://www.sciencedirect.com/science/article/pii/S2452302X17302905
Description
Summary:Summary: Even the most advanced drug-eluting stents evoke unresolved issues, including chronic inflammation, late thrombosis, and neoatherosclerosis. This highlights the need for novel strategies that improve stent biocompatibility. Our studies show that apolipoprotein A-I (apoA-I) reduces in-stent restenosis and platelet activation, and enhances endothelialization. These findings have therapeutic implications for improving stent biocompatibility. Key Words: apolipoprotein A-I, endothelialization, neointimal hyperplasia, platelet activation, stent biocompatibility
ISSN:2452-302X

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