Abstract
Clinical imaging of atherosclerotic plaques is based on anatomical demonstration of the narrowing of the involved artery (1). Angioscopy (2) and intravascular ultrasound (3) can demonstrate the precise location of the lesions, the extent of luminal narrowing and plaque thickening. However, both methods are invasive and cannot provide the composition or the metabolic status of the atherosclerotic lesion (4). Plaques rich in macrophages and foam cells may denote high risk of plaque rapture (5) whereas fibrous plaques may denote slowly emergent lesions. Lesions rich in actively proliferating smooth muscle cells may be an indication of accelerated luminal diameter reduction (6). Other targets that might have potential applications may be associated with neoantigens that are expressed due to microvascular injury inherent in atherogenesis. Therefore, targeting macrophage, foam cell hyper-accumulation or hyperactivity intravascularly, neoexpression or hyperexpression of various vascular adhesion molecules, or the metabolites that may be incorporated into the cellular components of the atherosclerotic lesions may provide novel and specific diagnostic and therapeutic applications.
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Khaw, BA. (2002). Targeting Atherosclerotic Plaques. In: Muzykantov, V., Torchilin, V. (eds) Biomedical Aspects of Drug Targeting. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-4627-3_4
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DOI: https://doi.org/10.1007/978-1-4757-4627-3_4
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