Chertok V M, Zakharchuk N V, Chertok A G
Pacific State Medical University, Vladivostok, Russia.
Zh Nevrol Psikhiatr Im S S Korsakova. 2017;117(8. Vyp. 2):43-55. doi: 10.17116/jnevro20171178243-55.
This review presents the data on cellular and molecular mechanisms of angiogenesis regulation linked to the vascular epithelium. According to current conceptions, activated endothelial cells and their predecessors (progenitor cells) are involved in the regulation of angiogenesis. These cells synthesize angiogenic molecules differing by the chemical structure and mechanism of biological effect and allowing a direct or indirect control over each stage of angiogenesis. Both the excess and insufficient angiogenesis can lead to fast and irreversible changes in nervous tissue under certain conditions. For this reason, the balance in the system of molecular stimulators and inhibitors of angiogenesis is especially important for brain function. Without adequate reperfusion of an affected brain area the post-stroke neuroreparation, which can be provided with timely stimulation of angiogenesis, is unattainable and the intensification of this process in tumors, on the contrary, has adverse consequences. Growth of a tumor and its metastatic spread are substantially associated with an increase in the level of tumor tissue vascularization, and blocking angiogenesis is often the only productive way to limit the growth of a tumor. However our knowledge of mechanisms of angiogenesis regulation in the brain on the cellular and molecular level in physiological and pathological conditions is still insufficient, and, therefore, the influence of angiogenic factors on tissue targets do not always cause the expected effects.
本综述介绍了与血管内皮相关的血管生成调节的细胞和分子机制的数据。根据目前的概念，活化的内皮细胞及其前体细胞（祖细胞）参与血管生成的调节。这些细胞合成的血管生成分子在化学结构和生物学效应机制上有所不同，并能对血管生成的每个阶段进行直接或间接控制。在某些情况下，血管生成过多或不足都会导致神经组织快速且不可逆的变化。因此，血管生成分子刺激剂和抑制剂系统的平衡对脑功能尤为重要。如果受影响的脑区没有足够的再灌注，中风后的神经修复（可通过及时刺激血管生成来实现）将无法实现，相反，肿瘤中这一过程的强化会产生不良后果。肿瘤的生长及其转移扩散与肿瘤组织血管化水平的增加密切相关，而阻断血管生成通常是限制肿瘤生长的唯一有效方法。然而，我们在细胞和分子水平上对生理和病理条件下大脑中血管生成调节机制的了解仍然不足，因此，血管生成因子对组织靶点的影响并不总是产生预期的效果。
