Verjans Johan W H, van de Borne Susanne W M, Hofstra Leonard, Narula Jagat
Division of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Methods Mol Biol. 2011;680:227-35. doi: 10.1007/978-1-60761-901-7_15.
Myocardial fibrosis after myocardial infarction plays a major role in cardiac remodeling, development of heart failure, and arrhythmias. Both replacement and interstitial fibrosis are determined by the extent of myofibroblastic proliferation and hence the extent of collagen deposition. It is logical to propose that a molecular imaging strategy that is able to determine the rate of myofibroblastic proliferation should be able to foretell the magnitude of myocardial remodeling and the likelihood of development of heart failure. Of various plausible targets on the proliferating myofibroblasts, receptors for neurohumoral agonists and overexpression of integrin moieties may offer best options for molecular imaging. In this chapter we describe the assessment of angiotensin II receptor and αvβ3 integrin upregulation in a mouse model after myocardial infarction using real time in vivo fluorescence imaging and nuclear imaging.
心肌梗死后的心肌纤维化在心脏重塑、心力衰竭的发展以及心律失常中起主要作用。替代性纤维化和间质纤维化均由肌成纤维细胞增殖程度决定,进而由胶原沉积程度决定。由此推测,一种能够测定肌成纤维细胞增殖速率的分子成像策略应该能够预测心肌重塑的程度以及发生心力衰竭的可能性。在增殖的肌成纤维细胞上的各种可能靶点中,神经体液激动剂受体和整合素部分的过表达可能为分子成像提供最佳选择。在本章中,我们描述了使用实时体内荧光成像和核成像技术,在心肌梗死后的小鼠模型中评估血管紧张素II受体和αvβ3整合素上调情况。