Matsui Yutaka, Morimoto Junko, Uede Toshimitsu
Yutaka Matsui, Toshimitsu Uede, Department of Matrix Medicine, Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan.
World J Biol Chem. 2010 May 26;1(5):69-80. doi: 10.4331/wjbc.v1.i5.69.
After onset of myocardial infarction (MI), the left ventricle (LV) undergoes a continuum of molecular, cellular, and extracellular responses that result in LV wall thinning, dilatation, and dysfunction. These dynamic changes in LV shape, size, and function are termed cardiac remodeling. If the cardiac healing after MI does not proceed properly, it could lead to cardiac rupture or maladaptive cardiac remodeling, such as further LV dilatation and dysfunction, and ultimately death. Although the precise molecular mechanisms in this cardiac healing process have not been fully elucidated, this process is strictly coordinated by the interaction of cells with their surrounding extracellular matrix (ECM) proteins. The components of ECM include basic structural proteins such as collagen, elastin and specialized proteins such as fibronectin, proteoglycans and matricellular proteins. Matricellular proteins are a class of non-structural and secreted proteins that probably exert regulatory functions through direct binding to cell surface receptors, other matrix proteins, and soluble extracellular factors such as growth factors and cytokines. This small group of proteins, which includes osteopontin, thrombospondin-1/2, tenascin, periostin, and secreted protein, acidic and rich in cysteine, shows a low level of expression in normal adult tissue, but is markedly upregulated during wound healing and tissue remodeling, including MI. In this review, we focus on the regulatory functions of matricellular proteins during cardiac tissue healing and remodeling after MI.
心肌梗死（MI）发作后，左心室（LV）会经历一系列分子、细胞和细胞外反应，导致左心室壁变薄、扩张和功能障碍。左心室在形状、大小和功能上的这些动态变化被称为心脏重塑。如果心肌梗死后的心脏愈合过程不正常进行，可能会导致心脏破裂或适应性不良的心脏重塑，如左心室进一步扩张和功能障碍，最终导致死亡。尽管这一心脏愈合过程的确切分子机制尚未完全阐明，但该过程是由细胞与其周围细胞外基质（ECM）蛋白的相互作用严格协调的。细胞外基质的成分包括胶原蛋白、弹性蛋白等基本结构蛋白以及纤连蛋白、蛋白聚糖和基质细胞蛋白等特殊蛋白。基质细胞蛋白是一类非结构性的分泌蛋白，可能通过直接与细胞表面受体、其他基质蛋白以及可溶性细胞外因子（如生长因子和细胞因子）结合来发挥调节功能。这一小类蛋白质包括骨桥蛋白、血小板反应蛋白-1/2、腱生蛋白、骨膜蛋白以及富含半胱氨酸的酸性分泌蛋白，在正常成年组织中表达水平较低，但在伤口愈合和组织重塑（包括心肌梗死）过程中会显著上调。在本综述中，我们重点关注基质细胞蛋白在心肌梗死后心脏组织愈合和重塑过程中的调节功能。
