Department of Physiology and Pathophysiology, Institute of Cardiovascular Sciences, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada.
Adv Exp Med Biol. 2019;1132:35-41. doi: 10.1007/978-981-13-6657-4_4.
Cardiac muscle (the myocardium) is a unique arrangement of atria and ventricles that are spatially and electrically separated by a fibrous border. The spirally-arranged myocytes in both left and right ventricles are tethered by the component molecules of the cardiac extracellular matrix (ECM), including fibrillar collagen types I and III. Loss of normal arrangement of the ECM with either too little (as is observed in acute myocardial infarction) or too much (cardiac fibrosis in chronic post-myocardial infarction) is the primary contributor to cardiac dysfunction and heart failure. Matricellular proteins exist as non-structural signaling moieties in the ECM, and in the context of cardiac hypertrophy and heart failure, secreted 90 kDa periostin protein has attracted intense scrutiny during the past decade. Secreted periostin is now recognized for its important role in ECM development and maturation, as well as cellular adhesion. The novel mechanisms of periostin function include its role as a mediator of cell-to-matrix signaling, cell survival, and epithelial-mesenchymal transition (EMT). A number of recent studies have examined the hypothesis that periostin is a major contributor to ECM remodeling in the heart, and a number of very recent studies underscore its important role. This review examines recent developments in the mechanisms of periostin function in the normal heart and vasculature, and discusses recent advances which underpin its putative role in the development of cardiovascular disease. Periostin expression is very low at baseline in healthy tissues, but is re-expressed in damaged heart and in vessel walls after injury, in activated cardiac myofibroblasts and vascular smooth muscle cells, respectively. For this reason, periostin may be exploited for investigation of mechanisms of cardiac fibrosis , and we speculate that data generated from studies utilizing this approach may shed light on the timing for application of periostin-specific therapies to quell cardiac fibrosis and associated cardiac dysfunction.
心肌（心肌）是心房和心室的独特排列，通过纤维边界在空间和电上分开。左、右心室中的螺旋排列的心肌细胞被心脏细胞外基质（ECM）的组成分子束缚，包括纤维胶原 I 型和 III 型。ECM 的正常排列丧失，无论是太少（如急性心肌梗死中观察到的那样）还是太多（慢性心肌梗死后的心脏纤维化），都是心脏功能障碍和心力衰竭的主要原因。基质细胞蛋白作为 ECM 中的非结构信号部分存在，在心脏肥大和心力衰竭的情况下，分泌的 90kDa 骨膜蛋白在过去十年中受到了强烈关注。分泌的骨膜蛋白现在因其在 ECM 发育和成熟以及细胞黏附中的重要作用而得到认可。骨膜蛋白功能的新机制包括其作为细胞-基质信号转导、细胞存活和上皮-间充质转化（EMT）的介质的作用。最近的一些研究检验了这样一种假设，即骨膜蛋白是心脏 ECM 重塑的主要贡献者，而最近的一些非常新的研究强调了其重要作用。这篇综述检查了骨膜蛋白在正常心脏和脉管系统中的功能机制的最新发展，并讨论了支持其在心血管疾病发展中潜在作用的最新进展。在健康组织中，骨膜蛋白的基础表达水平非常低，但在受损的心脏和受伤后的血管壁中重新表达，分别在激活的心肌成纤维细胞和血管平滑肌细胞中。因此，骨膜蛋白可能被用于研究心脏纤维化的机制，我们推测，利用这种方法产生的数据可能会阐明骨膜蛋白特异性治疗方法的应用时机，以平息心脏纤维化和相关的心脏功能障碍。
