Bone marrow–derived hematopoietic stem/progenitor cells are vasculogenic and play an important role in endothelial health and vascular homeostasis by participating in postnatal vasculogenesis. Progenitor cells are mobilized from bone marrow niches in response to remote ischemic injury and migrate to the areas of damage and stimulate revascularization largely by paracrine activation of angiogenic functions in the peri-ischemic vasculature. This innate vasoprotective mechanism is impaired in certain chronic clinical conditions, which leads to the development of cardiovascular complications. Members of the renin-angiotensin system—angiotensin-converting enzymes (ACEs) ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and receptors AT1 and Mas—are expressed in vasculogenic progenitor cells derived from humans and rodents. Ang-(1-7), generated by ACE2, is known to produce cardiovascular protective effects by acting on Mas receptor and is considered as a counter-regulatory mechanism to the detrimental effects of Ang II. Evidence has now been accumulating in support of the activation of the ACE2/Ang-(1-7)/Mas receptor pathway by pharmacologic or molecular maneuvers, which stimulates mobilization of progenitor cells from bone marrow, migration to areas of vascular damage, and revascularization of ischemic areas in pathologic conditions. This minireview summarizes recent studies that have enhanced our understanding of the physiology and pharmacology of vasoprotective axis in bone marrow–derived progenitor cells in health and disease.

中文翻译：

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针对心血管疾病的血管祖细胞中的 ACE2/血管紧张素-(1-7)/Mas 受体轴。

骨髓来源的造血干/祖细胞是血管生成的，通过参与出生后的血管生成，在内皮健康和血管稳态中发挥重要作用。祖细胞从骨髓壁龛中动员出来，以响应远程缺血性损伤，迁移到损伤区域并主要通过缺血周围血管系统中血管生成功能的旁分泌激活来刺激血运重建。这种先天的血管保护机制在某些慢性临床疾病中受损，从而导致心血管并发症的发生。肾素-血管紧张素系统的成员——血管紧张素转换酶 (ACE) ACE 和 ACE2、血管紧张素 II (Ang II)、Ang-(1-7) 以及受体 AT1 和 Mas——在源自人类和啮齿动物。Ang-(1-7)，由ACE2生成，已知通过作​​用于 Mas 受体产生心血管保护作用，并被认为是 Ang II 有害作用的反调节机制。越来越多的证据支持通过药物或分子操作激活 ACE2/Ang-(1-7)/Mas 受体通路，刺激祖细胞从骨髓中动员、迁移到血管损伤区域和血运重建病理条件下的缺血区域。这篇小综述总结了最近的研究，这些研究增强了我们对健康和疾病中骨髓源性祖细胞血管保护轴的生理学和药理学的理解。越来越多的证据支持通过药物或分子操作激活 ACE2/Ang-(1-7)/Mas 受体通路，刺激祖细胞从骨髓中动员、迁移到血管损伤区域和血运重建病理条件下的缺血区域。这篇小综述总结了最近的研究，这些研究增强了我们对健康和疾病中骨髓源性祖细胞血管保护轴的生理学和药理学的理解。越来越多的证据支持通过药物或分子操作激活 ACE2/Ang-(1-7)/Mas 受体通路，刺激祖细胞从骨髓中动员、迁移到血管损伤区域和血运重建病理条件下的缺血区域。这篇小综述总结了最近的研究，这些研究增强了我们对健康和疾病中骨髓源性祖细胞血管保护轴的生理学和药理学的理解。