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Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype.
Vanags, Laura Z; Tan, Joanne T M; Galougahi, Keyvan K; Schaefer, Andreas; Wise, Steven G; Murphy, Andrew; Ali, Ziad A; Bursill, Christina A.
Afiliação
  • Vanags LZ; Immunobiology Group, The Heart Research Institute, Sydney, Australia.
  • Tan JTM; Sydney Medical School, University of Sydney, Sydney, Australia.
  • Galougahi KK; Immunobiology Group, The Heart Research Institute, Sydney, Australia.
  • Schaefer A; Sydney Medical School, University of Sydney, Sydney, Australia.
  • Wise SG; Center for Interventional Vascular Therapy, Columbia University, New York, New York.
  • Murphy A; Cardiovascular Research Foundation, New York, New York.
  • Ali ZA; Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
  • Bursill CA; Immunobiology Group, The Heart Research Institute, Sydney, Australia.
JACC Basic Transl Sci ; 3(2): 200-209, 2018 Apr.
Article em En | MEDLINE | ID: mdl-30062205
ABSTRACT
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2018 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2018 Tipo de documento: Article