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WIREs Nanomed Nanobiotechnol
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Current status of nanotechnology approaches for cardiovascular disease: a personal perspective

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Abstract Nanotechnology is poised to have an increasing impact on cardiovascular health in coming years. Diagnostically, multiplexed point‐of‐care devices will enable rapid genotyping and biomarker measurement to optimize and tailor therapies for the individual patient. Nanoparticle‐based molecular imaging agents will take advantage of targeted agents to provide increased insight into disease pathways rather then simply providing structural and functional information. Drug delivery will be impacted by targeting of nanoparticle‐encapsulated drugs to the site of action, increasing the effective concentration and decreasing systemic dosage and side effects. Controlled and tailored release of drugs from polymers will improve control of pharmacokinetics and bioavailability. The application of nanotechnology to tissue engineering will facilitate the fabrication of better tissue implants in vitro, and provide scaffolds to promote regeneration in vivo taking advantage of the body's own repair mechanisms. Medical devices will benefit from the development of nanostructured surfaces and coatings to provide better control of thrombogenicity and infection. Taken together, these new technologies have enormous potential for improving the diagnosis and treatment of cardiovascular diseases Copyright © 2009 John Wiley & Sons, Inc. This article is categorized under: Therapeutic Approaches and Drug Discovery > Nanomedicine for Cardiovascular Disease

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Illustration of processes of atherogenesis ranging from prelesional endothelial dysfunction (a) through monocyte recruitment to the development of advanced plaque complicated by thrombosis (b). The mechanisms are grossly simplified but focus on components (for example, cell adhesion molecules, macrophages, connective tissue elements, lipid core, and fibrin) and processes (for example, apoptosis, proteolysis, angiogenesis, and thrombosis) in plaques that have been imaged or that present useful potential imaging targets. ICAM, intercellular cell adhesion molecule; LDL, low‐density lipoprotein; MMP, matrix metalloproteinase; NO, nitric oxide; VCAM, vascular cell adhesion molecule. (Reprinted with permission. Copyright 2004 Macmillan Publishers Ltd.).

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Injection of nanofibers (NF) with platelet‐derived growth factor (P‐BB) decreases cardiomyocyte death after myocardial infarction (MI). Immunofluorescence staining of cleaved caspase‐3, a marker of apoptotic cell death was shown in sections from 1 day after injection of NFs with or without P100. Blue, DAPI (4′, 6‐diamidino‐2‐phenylindole, nuclear marker); red, α‐sarcomeric actinin; green, cleaved caspase‐3. Colocalization of caspase‐3 with cardiomyocytes is shown in yellow. Journal of Clinical Investigation. Online by Richard Lee. Copyright 2006 by American Society for Clinical Investigation. (Reprinted with permission 2006 American Society for Clinical Investigation).

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Protection of nanofibrous grafts from thrombus by MSCs in vivo. Mesenchymal Stem Cell (MSC)‐seeded grafts show greatly reduced platelet aggregation to the luminal graft surface (b) and thrombus formation (d) after 2 h compared to acellular grafts (a,c). After 60 days, a cellular grafts display intimal thickening (e, arrow), while MSC‐treated grafts do not (f). (Modified with permission. Copyright 2007 National Academy of Sciences, U.S.A).

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In vivo MRI of VCAM‐1 expression. (a) magnetic resonance imaging (MRI) before injection of VINP‐28. Dotted line depicts location of short‐axis view (insets, lower panel with color coded signal intensity). (b) Same mouse 48 h after injection of VINP‐28. A marked signal drop in the aortic root wall was noted(insets). The contrast‐to‐noise ratio (CNR) of the aortic wall was increased significantly after injection of the probe. (Reprinted with permission. Copyright 2006 Lippincott Williams and Wilkins).

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