Cardiomyocytes and Macrophages Discourse on the Method to Govern Cardiac Repair.
Cardiomyocytes and Macrophages Discourse on the Method to Govern Cardiac Repair.
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DOI：
10.3389/fcvm.2018.00134
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发表时间：
2018
影响因子：
3.6
通讯作者：
Silvestre JS
中科院分区：
文献类型：
--
作者：
Gomez I;Duval V;Silvestre JS
响应于病理生理应激，心脏组织经历深刻的重塑过程，其包括死亡驻留细胞的消除、功能性心肌细胞的代偿性肥大、血管隔室的生长和重塑以及纤维化瘢痕的形成。越来越多的证据表明，心脏重塑至少部分是由心肌细胞和巨噬细胞之间的复杂串扰控制的。大量的巨噬细胞靠近心肌细胞的战略位置表明，它们可以调节受损心脏中心肌细胞的命运。因此，巨噬细胞作为心肌细胞的关键支持细胞出现，并在心脏肥大、纤维化和重塑中发挥核心作用。值得注意的是，心脏组织通过驻留巨噬细胞的局部增殖以及血液来源的单核细胞的募集和分化来扩增心脏巨噬细胞的异质群体。也有人提出，心脏驻留巨噬细胞显示出与心脏组织中单核细胞衍生的巨噬细胞不同的功能特性。此外，巨噬细胞是通过调节动作电位扩散或心脏细胞周期折返对心脏传导或心肌细胞增殖具有非经典作用的生物实体的溢出来源。或者，应激的心肌细胞可以触发释放广泛的指示信号，这些信号可以调节巨噬细胞的数量，改变它们的表型，从而指导它们的有益或有害作用。在这篇综述中，我们强调了最近的发现，描述了心肌细胞和巨噬细胞之间的复杂对话如何在受伤的心脏组织中形成有害或愈合的信号机制。
In response to pathophysiological stress, the cardiac tissue undergoes profound remodeling process that incorporates the elimination of dying resident cells, compensatory hypertrophy of functional cardiomyocytes, growth and remodeling of the vascular compartment and formation of a fibrotic scar. Accumulating evidences indicate that cardiac remodeling is, at least in part, controlled by a complex crosstalk between cardiomyocytes and macrophages. The strategic location of abundant macrophages to the proximity of cardiomyocytes suggest that they could regulate the fate of cardiomyocytes in the injured heart. As such, macrophages appear as critical support cells for cardiomyocytes and play central roles in cardiac hypertrophy, fibrosis and remodeling. Notably, the cardiac tissue expands heterogeneous population of cardiac macrophages through local proliferation of resident macrophage as well as recruitment and differentiation of blood-derived monocytes. It has also been suggested that cardiac-resident macrophages display distinct functional properties from that of monocyte-derived macrophages in cardiac tissue. Furthermore, macrophages are an overflowing source of biological entities with non-canonical roles on cardiac conduction or cardiomyocyte proliferation by regulating action potential diffusion or cardiac cell cycle reentry. Alternatively, stressed cardiomyocytes can trigger the release of a broad repertoire of instructive signals that can regulate macrophage number, skew their phenotype and therefore direct their beneficial or deleterious actions. In this review, we highlight recent discoveries describing how the intricate dialogue between cardiomyocytes and macrophages can shape the deleterious or healing signaling mechanisms in the injured cardiac tissue.